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🏥 | Why "sleep" is so important for vaccination against viral diseases


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Why "sleep" is so important for vaccination against viral diseases

 
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In addition, it has a great influence on the immune function.
 

The corona (COVID-19) vaccine, which is currently the most important issue in the world.The elderly inoculation has settled down, and the next is younger ... → Continue reading

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Immune system

Immune system(Men-ekikei,English: immune system) Means in vivoPathogenNon-self substances such ascancer cellBy recognizing and killing abnormal cells and foreign substances such assickIt is a mechanism that integrates a large number of mechanisms to protect from. This mechanismウ イ ル スからParasiteIt senses and functions a wide range of pathogens and foreign substances while distinguishing them from the healthy cells and tissues of the living body itself. In the immune system細胞,組織,organAre precisely and dynamically linked.

In order to overcome this difficult task and survive, there is no single mechanism for recognizing and neutralizing pathogens.進化did.BacteriaSimple likeUnicellular organismBut,Innate immunityVirus calledinfectionDefend酵素I have a system. Other basic immune systems are ancientEukaryoteEvolved inplant,Fishes,Reptiles,昆虫Remains in. Innate immunity is called defensinAntimicrobial peptidesIs a mechanism that involves, a phagocytic mechanism,[1] Complement system.

Human capitallikevertebrateIt is,Acquired immunityWe have evolved a more complex defense mechanism called. Acquired immunity is of many typesproteinConsists of dynamic interactions of cells, organs and tissues.This adaptation processImmune memoryTo create. Immune memory created from an initial response to a particular pathogen results in an enhanced response to a second encounter with the same particular pathogen. This process of acquired immunityvaccineIt is the basis of inoculation.

When the immune system becomes abnormal, it becomes more susceptible to diseases (infectious diseases, autoimmune diseases, allergies). If the immune system is less active than normal, immunodeficiency disease can occur, leading to repeated infections and life-threatening infections. Immunodeficiency disease is like severe combined immunodeficiency diseaseGenetic diseaseIs the result ofRetro virusCaused by an infectionAcquired immunodeficiency syndrome (AIDS)MedicineIs the cause. On the contrary, when the immune system is overactive,Autoimmune diseaseIs awakened. This results from increased immune system activity that attacks normal tissues as if they were alien species. As a common autoimmune diseaseRheumatoid arthritis,Systemic lupus erythematosus(Also with lupus erythematosus),Type I diabetes, There is. Allergies are called hypersensitivity and are caused by an excessive immune response.組織Damage to.AnaphylaxisThere is a shock and so on.

ImmunologyIs in all areas of the immune systemResearchCovering and humanHealthAnd is deeply related to illness. Further research in this area is to promote health and illness.治療Can also be expected.

Overview

What is immunity?Human capital,Animal"Different from myself" that has entered the bodyforeign body”(Non-self) of the living bodyHomeostasisIt is one of the maintenance mechanisms. In general,Drug,Chemical substanceTo eliminate suchliver Of酵素bymetabolismWorks, while immunity is better than thatHigh molecularIsprotein(Snake venom,Bee venomEtc.) and invaded the bodyPathogenOften works as a mechanism to eliminate. Especially due to pathogensinfectionIt is important as an infection defense mechanism to protect yourself from protection, and when simply called "immunity", this isInfection protection immunityOften refers to.

The immune systemInnate immunity(Congenital immunity, innate immunity,en: innate immune system)WhenAcquired immunity(Acquired immune system, adaptive immune system,en: adaptive immune system) And. Special in innate immunity細胞They are equipped with intruders that reproduce themselvesHostDiscover and eliminate pathogens in the body before they cause serious damage toProliferationIt can be dealt with before it causes serious harm to the host.

Acquired immunityantibody,complementDue to blood proteins such asHumoral immunitylymphocytesSuch as細胞byCellular immunityIs carried by. For lymphocytesDifferentiationMatureImmunoglobulinTo produceB cellsIn addition to the,ThymusDifferentiate withmatureToT cellsand so on. Other,PhagocytosisByantigenIs taken up, decomposed and presented to T cellsDendritic cellsEtc. are also involved in the expression of immune function. These cellsBone marrowProduced in the thymus andLymph node,spleenIt comes to function through interactions in lymphoid tissues such as.

The magnitude of the effect of both innate immunity and acquired immunity is self and non-self.分子It depends on whether the immune system has the ability to distinguish between the two. A self-body element that can be distinguished from foreign substances by the immune system.[2].. Foreign molecules that are distinguished from foreign substances by the immune system are called non-self molecules. One of the non-self molecules isantigen(Antigen; this isantibody gene(Abbreviation for erator), specific immunityReceptorDefined as a substance that binds to and induces an immune response[3].

Multi-layered defense

The immune systeminfectionProtects the living body with a multi-layered defense system while increasing its specificity. The simplest is the epithelial barrier,Bacteria,ウ イ ル スIs to prevent the invasion of the living body. PathogenWhen innate immunity (also called innate immunity) breaks through this barrier and invades the body, it is immediately detected and non-specifically eliminated. Innate immunity is everythingplantandAnimalRecognized in[4].. But if the pathogen escapes innate immunity wellvertebrateUnleashes a third-tier defensive reaction. This isAcquired immunityIt is activated by innate immunity once it comes into contact with the source of infection.The acquired immune system recognizes and attacks pathogens, but adapts its response to improve awareness of pathogens during infection.This mechanism remains in the immunological memory after the pathogen is eliminated, and is then strengthened each time the same (or very similar) pathogen is encountered, resulting in a faster and more powerful attack.[5].


Components of the immune system
ItemInnate immunityAcquired immunity
PathogenantibodyReaction ofNon-specific Non-specificSpecific
Time to maximum response after contactEliminate before contactShort (immediately)The first time is long (delayed to adapt to the pathogen), the second time is short (immediately)
Ingredients involvedCellular immunityCellular andHumoral immunity
Cell nameEpithelialWhite blood celllymphocytes
Immune memoryNoneNone (Immune memory #Innate immune memory)Yes
Distribution in the living worldAlmost all living thingsAlmost all living thingsVertebrates with jaws

Epithelial barrier

PathogenCells exposed toEpithelial(So-called皮膚だ け で な く,Mucosa,IntestineEtc.)Living bodyTheinfectionIt has a barrier that protects it from mechanical, chemical and biological protection.Surface barrier(en: Immune system #Surface barriers) Also.

Mechanical barrier

leafWaxiness seen inCuticle,昆虫 OfExoskeletonWas borneggShell ofmembraneAnd皮膚.. These are examples of mechanical barriers and are at the forefront of the line of defense against infection.[3].. The skinEpithelial, Outer layer,Genuine LeatherIt is composed of and mechanically blocks most infectious agents.

Howeverlung,IntestinesOperate other systems to protect openings that communicate with the outside world, such as the urinary tract. For example, with the lungstracheaThen,cough,sneezeWith the airflowCiliaBy the movement of, The urinary tractPee, Respiratory organs (such as the nasal cavity and respiratory tract) and digestive organs (such as the oral cavity and gastrointestinal tract) due to mucusmicroorganismCatch and entangle[6].

Chemical barrier

Chemical barrierinfectionWork for defense.皮膚It is,keratinRich in細胞Are closely arranged side by side. This isWedPlay the skinWeakly acidicTo keep the skinBacteria OfProliferationIt also works as a chemical barrier to suppress. Skin andBreatheThe tube is like β-defensinAntimicrobial peptidesSecrete[7]. saliva,,BreastmilkincludeLysozyme,Phospholipase A2Etc.酵素AlsoAntibacterialAn antibacterial substance that acts[8][9]. Vaginal discharge TheMenstruationEven slightly laterAcidicActs as a chemical barrier when leaning towardssemen ThePathogenKillingSpermine,Defensin,zincincluding[10][11]. Secretory fluidAsGastric juiceToStomach acidIs extremely lowpHWhile showingdigestive enzyme OfProteolytic enzymeIt has a strong chemical defense against ingested pathogens.

Biological barrier

ReproductionUreter,StomachIn the tubeSymbiosisdoingBacteriaPlexusPathogenNutrientsAnd breeding groundsPathogenCompete with and act as a biological barrier. in this case,pHAnd availableionlikeEnvironmentMay change[12].. This means that the pathogenOnsetUp to possible populationProliferationReduce the chances of being able to do it.IntestinesWithinIntestinal bacteriaIs working.YogurtUsually included inLactic acid bacteriaPure likecultureReintroduction of benign flora by children's intestinal tractinfectionAtmicroorganismBalance the groupHealthThere is evidence that it works to help keep things clean. This is bacterialGastroenteritis,Inflammatory bowel disease,Urinary-tract infectionGives hope to preliminary data on postoperative infection studies[13][14][15].

BacterialInfectionOften againstAntibioticsIs used, but most antibiotics act non-specifically on both pathogenic and normal bacteria,MoldIt doesn't work for antibioticsOral administrationByFungusAbnormally proliferates and vaginaCandidiasislikeMycosisMay cause[16].

Innate immunity

Pathogen EpithelialBreak through the barrier atmicroorganism,toxicityIf a substance can successfully enter the living body, then in the living bodyInnate immune systemConfront (congenital immune system). This is due to humoral, chemical and cellular barriersHostIt is a protection mechanism of.White blood cellAnd lymphocytes細胞And mechanisms are mobilized to protect the host, usually at that timeInflammatory reactionOccurs. In this innate immune response, the living body usually structures microorganisms.Pattern recognition receptorIt is activated when it is detected by. This structural pattern is conserved among a wide range of microbial groups[17].. Alternatively, the cell gives a warning signal when it is damaged. Many, but not all, of them are the same that recognize pathogensReceptorPerceived by[18].. Protected by the natural immune system is a comprehensive response to pathogens[3]..In other words, instead of responding to various pathogens separately, they always deal with them in a general-purpose manner, so the time to activate their effects is short, so to speak, they are always ready for battle.On the other hand, there is no immune memory like the acquired immune system, and it is not a mechanism to protect for a long time.

The natural immune system is the main system of host defense for most organisms[4],plant-Fungi-昆虫-Multicellular organism(mammalianHigher such asvertebrate(Except) is the main defense system. It also has a primitive life,進化It is considered to be an old defense method. Also,Toll-like receptor, Nod protein,RIG-I(PathogenesismicroorganismResearch on sensors for) has progressed since the end of the 20th century, and innate immunity has been promoted.Higher animalsIt is an important mechanism as a premise for the establishment of acquired immunity (for example).Macrophage,Dendritic cellsIs directly activated by the presence of the pathogen).

Fluid or chemical barrier

Inflammation

Inflammation ThePathogen OfinfectionIs one of the first responses of the immune system to or stimuli[19].. Signs of inflammation are ...pain,swellingOne of the組織Inflow tobloodCaused by an increase in.

InflammationinjuryOr infected細胞 secretionToEicosanoidCytokineIt is caused by chemical factors such as a specific group called, which is the normal response of the immune system to infection. For eicosanoidsProstaglandinIncludes, if this substance is associated with inflammation, with feverBlood vesselCause expansion. Also included in eicosanoidsLeukotrieneIs a kind ofWhite blood cellActs on (lymphocytes)[20][21].. For the types of cytokinesWhite blood cellInvolved in communication betweenInterleukin,ChemotaxisPromptMacrophageAnd so onChemokine, Of the host cellProtein synthesisLike stoppingウ イ ル スHas antiviral activity againstinterferonand so on[22].. Growth factors andCytotoxicityFactors toosecretionMay be done. These cytokines and otherChemical substanceMobilizes immune cells to the site of infection, eliminates pathogens, and then in any tissue damagedrepairUrge[23].

Complement system

Complement systemIs a biochemical cascade that assists (supplements) the antibody's ability to attack the surface of foreign cells or index them to be destroyed by other cells. What is complement?antibodyAuxiliary or complementary to the function ofproteinIs. More than 20 proteins involved, depending on the antibodyPathogenKillSupplement It was named to mean that it has the ability to strengthen. Complement is a major factor in the innate immune responsebody fluidMake a sexual element[24][25].. Many species have a complement system,mammalianNot onlyplant,Fishes,InvertebrateSomewhat primitive, such as part ofBiology But i have[26].

Human capitalSo this response is thesemicroorganismBy the binding of complement to the antibody attached to the microorganism, or on the surface of the microorganismcarbohydrateBy binding the complement protein toactivationWill be done. This cognitive signal triggers a prompt killing response[27].. It is the degree of signal enhancement caused by the subsequent activation of complement molecule proteolysis that determines the speed of the response. When many complement proteins are activated by proteolytic cleavageProtease(Proteolytic enzyme). After the complement protein attaches to the microorganism, the complement's own proteolytic enzyme activity is expressed, followed by activation of other complement proteolytic enzymes, which occurs continuously. this isCatalytic reactionCauses a cascading and positive first signalfeedbackIt is to strengthen while controlling with[28].. By the complement clinging in this wayCell membraneIs destroyed and the pathogen is killed[24].. Often due to complement activationinfectionCellularProtoplasmDestruction occurs, resulting in infected cellsDissolution, Causes the death of pathogens. The end product of the complement mechanismC5b6789Is another nameCell membrane damage complexIt is also called by destroying the infected cells and the cell membrane of the source of infection.,LysisWake up. thisImmunolytic phenomenonOrImmunolytic reactionIn the defense against bacteriaNeutrophilIt is an important mechanism along with the phagocytosis of. CascadepeptideTo attract immune cells,Blood vesselUpdates the permeability of the pathogenOpsonization(Coat) and mark it so that it can be destroyed. The complement system opsonizes (or coats) the surface of the pathogen, tagging it so that it is destroyed by other cells, inducing recovery of inflammatory cells, and neutralizing antigenic antibodies. Remove the complex debris.

Cell barrier

White blood cellWhichorgan,組織Not combined with, but a single細胞It is an organ consisting of and is independentUnicellular organismThe right arm of the innate immune system, which behaves like[3].. White blood cells of the innate immune system include mast cells, eosinophils, basophils, natural killer cells,PhagocytesIt has the ability to identify (macrophages, neutrophils, dendritic cells) and pathogens that can induce infection. These cellsPathogenRecognize and eliminate,microorganismSwallow and kill, or contact and attack larger pathogens[26].. Innate immunity works in the first stages of infection, but many sources have developed strategies to avoid innate immunity. Natural immune system cells are more important in specific adaptive acquired immunityMediatorIs[5],Antigen presentationIt can be activated by going through a process known as.

The phagocytic function plays an important role in cellular innate immunity and is performed by cells called phagocytic cells that swallow and eat pathogens and granules. Phagocytes phagocytose sources of infection and particles, ieEatIt plays a role of eliminating by doing so. Phagocytes usually circulate in the body looking for pathogens,CytokineGuided to a specific site by[3].. Once the pathogen is swallowed by phagocytes, it is intracellular called fargosome.VesicleCaptured by, followed byLysosomeIt fuses with another vesicle called to form a far lysosome. The pathogen isdigestive enzymeBy orBreatheFollow the burstFree radicalsKilled by release into fargolysosomes[29][30].. The phagocytic function has evolved to acquire nutrients, but in phagocytes this role has been expanded to act as a defense mechanism that includes pathogen phagocytosis.[31].. The phagocytic function is that phagocytesvertebrateAlsoInvertebrateProbably the oldest form of host defense, as it is also present in[32].

Neutrophils and macrophages are phagocytes that move throughout the body in search of invading pathogens.[33].. On macrophages and neutrophilsReceptorToBacteriaBacterial phagocytosis and destruction begin when molecules bind.

Neutrophil
usuallyBlood flowIt exists inside and is the most abundant among phagocytes. Usually accounts for 50% to 60% of total circulating leukocytes[34].. Especially as a result of bacterial infectionInflammationNeutrophils in the acute phaseChemotaxisIt moves to the inflamed area by the process. In most cases, it is the first cell to arrive at the site of infection.
Macrophage(Macrophage)
Tracking the source of infection that exists throughout the organization組織And put it in the intercellular space. With versatile cells酵素,complementProtein, andInterleukin-1Wide range of control factors such asChemical substanceTo produce[35].. Macrophages are corpses and dumpster diving (Scavenger) Also acts as a cell, removing useless cells in the body and other decaying deposits and activating the adaptive immune systemAntigen presenting cellsWork as[5].
Dendritic cells(DC; dendritic cell)
Get in touch with the outside world組織It is a phagocyte that exists in. Therefore, this cell is mainly皮膚,nose,lung,stomach,IntestinesExists in[36].. The name of this cell isNerve cell OfDendriteIt was named because it resembles (dendrite). Both nerve cells and dendritic cells have many dendrites,NerveNot involved in function. Dendritic cells are the key to the adaptive immune systemT cellsSince it presents an antigen to the immune system, it bridges innate immunity and acquired immunity.[36].
Natural killer cells(NK cells)
tumorCellular and viral infectionsGlandular cellsAttack and destroy[37](By the way, this is not included in the inflammatory reaction).
BasophilEosinophil
Related to neutrophils,ParasiteChemistry in defense againstMediatorThesecretionTo do. Also,asthmaSuch asAllergiesAlso involved in[38].
Mast cells(Mast cell)
Connective tissue,MucosaExists in infection protection andRecovery,InflammationControl the response[39].. This cell is the mostAllergiesAnaphylaxisBe involved in[34].

Specific and adaptive acquired immunity

Acquired immune systemIs the earlyvertebrateTo進化And cause a stronger immune response, individualPathogenIndicates that is of a particular typeantigenIt is a mechanism that discriminates and memorizes (immune memory) by[40].. The response is antigen-specific andAntigen presentationIt is necessary to recognize that it is a specific non-self antigen during the process called. Recognition of antigen specificity allows the activation of a coordinated response to a particular pathogen or cells infected with a particular pathogen. The ability to initiate such a coordinated response is retained by memory cells in the body. If the pathogen hits the body more than onceinfectionIf so, these specific memory cells are used to immediately eliminate the pathogen.

lymphocytes

Involved in acquired immunity細胞Is of a particular typeWhite blood cellso,lymphocytesIt is called. Its main type isB cellsT cellsAndBone marrowInHematopoietic stem cellsDerived from[26].. B cellsHumoral immunityInvolved in the reaction, T cellsCellular immunityInvolved in the response. B cells and T cells recognize specific goalsReceptorHas a molecule. To recognize targets of "foreign bodies" such as pathogens, T cellsantigen(Pathogen) Is disassembled into small piecesSelfReceptorMajor histocompatibility complex(MHC,Major Histocompatibility Complex) Must be presented in combination with the molecule. For T cellsCytotoxic T cells(Killer T cells)Helper T cellsThere are two main subtypes. Cytotoxic T cellsMHC class I moleculeRecognizes only antigens bound to and helper T cellsMHC class II moleculeRecognizes only antigens bound to.These twoAntigen presentationMechanism reflects the different roles of the two types of T cells. As the third minor subtype of T cellsγδ T cellsRecognizes unprocessed antigens that do not bind to MHC receptors[41].

In contrast, B cell antigen-specific receptors are on the B cell surface.antibodyIt is a molecule that recognizes the entire pathogen without antigen processing. Antibodies on B cells are samples of antibodies that the B cells will produce in the future, but there are some differences. Each B cell proliferation system expresses a different antibody, and a complete set of B cell antigen receptors represents all the antibodies the body can make.[26].

Cytotoxic T cells (CTL)

Cytotoxic T cells(CTL, killer T cells)T cellsIn the subgroup ofウ イ ル ス(And otherPathogen)infectionDamaged, damaged, or dysfunctional細胞Kill[43]. B cellsLike, each type of T cell is differentantigenRecognize. Cytotoxic T cells are their own T cellsReceptor(TCR) Is another cellMHCIt is activated when it binds to a specific antigen that is complexing with a class I receptor. Recognition of this MHC-antigen complex is on T cellsCD8Helped by a co-receptor called. The T cells then migrate throughout the body in search of cells expressing MHC class I receptors that carry such antigens. When activated T cells come into contact with such cells,(English editionlikeCell injuryRelease the substance. Perforin is the target cellCell membraneMake a hole inion,water andtoxinInvade. (English edition(Proteolytic enzyme) Invasion of other toxic substances into target cellsApoptosisInduce[44].. Depends on T cellsHostCell killing is especially important in preventing viral replication. T cell activation is tightly regulated and is generally a very strong MHC-antigen complex activation signal.Helper T cellsRequires an additional activation signal by[44].

Helper T cells (Th)

Helper T cells(Th cells) regulate the immune response of both innate and adaptive immunity, and the body is specific.PathogenHelps determine which immune response to the[45][46]..Helper T cells have no ability to damage cells, do not kill dysfunctional cells, and do not directly eliminate pathogens.Instead, it controls the immune response by directing instructions to other immune cells.

Helper T cellsMHCBound to a class II moleculeantigenT cells that recognizeReceptor(TCR)Manifestationdoing. The MHC-antigen complex is the same helper T cellCD4Intra-T cells that are also recognized by co-receptors and act on T cell activation分子(For example(English edition) Is mobilized. The relationship between helper T cells with MHC: antigen complexCytotoxic T cellsWeaker. It is that cytotoxic T cells are activated by the intersection of one MHC: antigen complex molecule, whereas helper T cells are activated by a large number (about 1 to 200) of receptors, MHC: It means that the antigen complex must adhere. Also, for activation of helper T cells,Antigen presenting cellsAnd requires longer fellowship time[47].. Resting helper T cells affect the activity of many other cell types by activationCytokineFree. Cytokine signals released by helper T cells are macrophage signals.microorganismKilling and cytotoxic T cellsantibodyTo produceB cellsStrengthen the activities of[3].. In addition, helper T cell activation is a CD40 ligand (also known as CDXNUMX ligand).(English edition) Causes an increase in the amount of regulation of molecules expressed on the surface of T cells. This molecule acts as a typical additional stimulus signal required to activate antibody-producing B cells.[48].

γδ T cells

γδ T cellsIs a CD4+And CD8+Another T cell as opposed to a (αβ) T cellReceptorHelper T cells with (TCR),Cytotoxic T cells,andNK cellShare the same properties as. The conditions for obtaining a response from γδ T cells have not been completely elucidated. A subset of T cells with other unfamiliar mutant TCRs, such as CD1d-restrictiveNatural killer T cellsIt straddles a wide range between innate immunity and adaptive immunity.[49].. On the other hand, γδ T cells are TCR.geneIt is an element of adaptive immunity because it can reorganize to produce receptor diversity and also develop memory phenotypes. On the other hand, various subsets have restricted TCR or NK receptors.Pattern recognitionIt is part of the innate immune system because it may be used in. For example, a very large number of human Vγ9 / Vδ2 T cellsmicroorganismCommon produced by分子Respond within a few hours. More highly restricted Vδ1+ T cellsEpithelial cellsSeems to respond to the stress[50].

B cells and antibodies

1B cellsIs on the surfaceantibodyIs a specific outpatientantigenWhen combined withPathogenWill be recognized[51].. This antigen / antibody complex is taken up by B cells and is a proteinbreak downBy processpeptideBe made. B cells then specificize these antigenic peptidesMHCPresented on a class II molecule. The complex of MHC and antigen specifically binds to that antigenHelper T cellsAnd its helper T cells activate B cellsLymphocainEmit[52].. When B cells are activated and begin to divide for proliferation, their offspring (Plasma cells) Have millions of specific antibody copies that recognize this antigen分子Also produces and secretes.

These antibodiesBlood vesselPlasma andLymphatic vesselsEnter and circulate.antibodyThe substance ofImmunoglobulinCalledproteinIs expressing the antigenBacteriaIt specifically binds to pathogens such asComplement systemActivation orPhagocytesMark for uptake and destruction by. thisOpsonizationThat is. Antibodies are bacterial against invading pathogenstoxinOr combine withウ イ ル スDirectly by interfering with the receptors used by bacteria and bacteria to infect cellsneutralizeCan also be[53].

Alternative adaptive immune system

Classic of adaptive immunity分子(For exampleantibody,T cellsReceptor)Vertebrates with jawsDespite being only presentLamprey,EelPrimitive jawless likevertebrateA unique lymphocyte-derived molecule has been found in. These animals carry a large group of molecules called mutant lymphocyte receptors (VLRs), which are jaw-bearing vertebrate antigens.ReceptorOf a very small number (1 or 2) likegeneProduced only from. These molecules are in the same way as antibodiesPathogen OfantigenIs believed to bind to antibodies with the same degree of specificity[54].

Immune memory

B cellsT cellsRemains in the body for a long period of time in those progeny cells when they are activated and begin to replicateMemoryThere will be something that will become a cell.AnimalThroughout their lifetime, these memory cells are unique to eachPathogenIt retains the memory of encountering the pathogen and can trigger a powerful response when the pathogen is detected again. This is due to the pathogen throughout the life of the individualinfectionIt can be said to be "adapted" because it occurs in adaptation to and the immune system prepares for future contact.Immune memoryCan hold either in the form of short-term passive memory or in the form of long-term active memory.

Passive memory

Passive immunity passive immunity It is,antibody,Cytotoxic T cellsAn immune response caused by administration of an existing agent such as (CTL).

NewbornIn advancemicroorganismEspecially without contactinginfectionEasy to receive. There, the mother provides several levels of passive defense.妊娠Special type of medium antibodyIgG placentaDirectly from the mother viaFetusWill be shipped to. ThereforeHuman capitalNewbornBirthAlready have antibodies with the same range of antigen specificity as high-level mothers[55].BreastmilkAlso has antibodies in the babystomachTo protect against bacterial infections until the newborn can synthesize its own antibodies[56].. This passive immunity is usually short-lived and lasts only days to months, because the fetus does not actually make memory cells or antibodies and only borrows them from the mother.Medical scienceSo, defensive passive immunity is antibody-rich from one individual to anotherserumCan also be done by artificially transferring[57].

Active memory and immune treatment

Active immunity active immunity It is,vaccineSuch asantigenImmune response induced by administration.

long-termActiveMemory is after infectionB cellsandT cellsObtained by activation of. Active immunity is an artificial vaccineVaccinationCan be established by. The principle of vaccination (or called immune treatment) isPathogenIs to introduce the antigen of the immune system to stimulate the immune system to develop specific immunity against the specific pathogen and prevent the disease caused by the pathogen.[3].. This deliberate induction of the immune response has been successful by leveraging the naturally occurring specificity of the immune system and thus being able to induce immunity.Human capitalOne of the leading causes of death in the populationInfectionVaccine treatment is one of the most effective manipulations of the immune system developed by mankind.[58][26].

Most viral vaccines are based on live attenuated viruses, but many bacterial vaccines have no adverse effectspoisonIngredients of substances, etc.BacteriaBased on the non-cellular components of the components of[3].. Most bacterial vaccines are innate immune, as vaccines with antigens derived from many non-cellular components do not produce much adaptive immune response.Antigen presenting cellsTo activate and maximize immunogenicityAdjuvantProvided with the addition of[59].

Human immune disorders

The immune system has taken up specificity, inducibility, and adaptability to have a highly effective structure. However, host defense can fail, which can be divided into three broad categories. Immunodeficiency, autoimmunity, hypersensitivity.

Immunodeficiency

Immunodeficiency occurs when one or more elements of the immune system fail. The immune systemPathogenThe ability to respond to is diminished young and old. Immune response is immune from around 50 years oldAgeingBegins to decline for[60][61].Developed countryThen.obesity,Alcoholism,DrugUse is a common cause of weakening immune function[61].. HoweverDeveloping countriesThen.MalnutritionIs the most common cause of immunodeficiency[61].. enoughproteinDo not takediet TheCellular immunity,complementActivity,Phagocytesfunction,IgAAntibody concentration,CytokineImpair production.NutrientsIsion,copper,zinc,selenium,vitaminA, C, E, B6,Folic acid(Vitamin B9) Is deficient in the immune response[61].. Plus when you are youngThymusTheHeredityOfmutationIs the cause of手術Loss of removal by means of severe immunodeficiency and very high infectivity[62].

Immunodeficiency is hereditaryAcquiredBut it can happen[3].. ChronicGranulomasIn illnessPhagocytesMay have weak pathogen destructive power, but hereditary orCongenitalAIDS and some examples of immunodeficiencycancerType causes acquired immunodeficiency[63][64].

Kind ofウ イ ル スImmune function is destroyed by infection with variousInfection-complicationsIllness that causesAcquired immunodeficiency syndrome(AIDS, AIDS). Also this virusHuman immunodeficiency virus Called (HIV). Immune function is congenitally disrupted, and diseases that cause various infectious diseases are collectivelyPrimary immunodeficiency syndromeCalled.

Autoimmunity

Enhanced immune response is one extreme of immunodeficiency, especially autoimmune diseases. Here, the immune system cannot accurately distinguish between self and non-self, and the body part of itselfattackTo do. Many under normal conditionsT cellsTheantibodyIs selfpeptideReact with[65].. special細胞(ThymusandBone marrowOne of the functions of (hidden in) is to present autoantigens produced in the body to young lymphocytes and eliminate cells recognized as autoantigens to prevent autoimmunity.[51].

Hypersensitivity

Allergies (hypersensitivity) are self組織It is an immune response that damages the body. According to the Coombs classification, it can be divided into five types.

Type I allergy is an immediate reaction orAnaphylaxisThe reaction is often associated with allergies. Symptoms from mild discomfortdeadWide range up to. Type I allergyMast cells,BasophilSecretesIgEIs the cause[66].

Type II allergyantibodyOf its own cellsantigenToCombineIt comes from marking it to destroy it. this isAntibody-dependent enhancement of infection(ADE:British: Antibody-dependent enhancement, Cytotoxic hypersensitivity),IgG,IgMThe antibody is the cause[66].. Immune complex (antigen aggregation,complementDeposits of proteins, and IgG and IgM antibodies) in various tissues trigger a type III allergic reaction[66].

Type IV allergies (also known as cell-mediated or delayed allergies) usually take 2-3 days to develop. Type IV reactions are associated with many autoimmune diseasesInfectionSeen inContact dermatitis(IvySumac) May also be seen. It is the ones involved in these reactionsT cells, Monocytes andMacrophageIs[66].

Type V allergies have a similar mechanism to type II, except for the irritating part.Graves' diseaseIs a typical disease.

Other mechanism

InvertebrateDoes not produce lymphocytes andantibodyThe multi-element adaptive immune system is the first because it does not produce a humoral response based onvertebrateSeems to have occurred in[1].. However, many species utilize the mechanisms expressed as precursors to these aspects of vertebrate immunity. The immune systemBiology Seems to be even the simplest functional structure of.Bacteria TheBacteriophageと 呼 ば れ るウ イ ル スIt uses a unique defense mechanism called a restriction modification system to protect it from pathogens.[67].ProkaryotesAlso has an acquired immune system and has contacted in the pastPhage OfgenomeTo hold the fragmentCRISPRUsing an arrayRNA interferenceCan interfere with virus replication in the form of[68][69].

Pattern recognitionReceptorPathogenAccompanying分子It is used by almost all living things to detect. Called a defensinAntimicrobial peptidesIs all animals andplantOf the innate immune response seen in進化Is one of the elements preserved[1].Complement system,PhagocytesIs also used in most invertebrates.RibonucleaseAnd RNA interference reaction pathways are allEukaryoteIt is conserved in and is thought to play a role in the immune response to the virus.[70].

Unlike animals, plants lack phagocytes. Most plant immune responses have systemic chemical signals released by the plant[71].. When a part of a plant is infected, the plant undergoes a local hypersensitivity reaction. As a result, the cells at the infected site are swift.ApoptosisAnd prevent the spread of infection to other plants.Systemic acquired resistance(SAR; Systemic Acquired Resistance) is a type of defensive response that allows the entire plant to resist certain infectious agents.[71].. RNASilencingThe mechanism is particularly important for this systemic response as it can block viral replication.[72].

Tumor immunity

For other important roles of the immune systemtumorMay be found and eliminated. Tumor-transformed cells are normal細胞Not inantigenIs expressed. These antigens appear non-self to the immune system, and immune cellsTransformationAttacks tumor cells. By tumorManifestationThere are several sources of antigens to produce.Cervical cancerCauseHuman papillomaviruslikeCarcinogenic virusDerived[74][75].. Others are found only at low levels in normal cells, but self as seen at high levels in tumor cellsproteinIs. As an exampleTyrosinaseと 呼 ば れ る酵素There is some kind of expression when it is expressed at high levels皮膚Cells (egMelanosite)MelanomaConvert to tumor cells called[76][77].. The third possible source of tumor antigens is cells in normal cellsProliferationAnd proteins important for controlling survival are commonmutationTurns into a cancer-inducing molecule[74][78][79].

The main reaction of the immune system to tumors is abnormal cellsCytotoxic T cells(CTL) and sometimesHelper T cellsIs to destroy with the assistance of[77][80].. Tumor antigens are similar to viral antigensMHCPresented on class I molecules. This causes cytotoxic T cells (CTL) to consider tumor cells as abnormal.[81].NK cellSimilarly, it kills neoplastic cells and acts especially on tumor cells in which MHC class I molecules are expressed less than normal. This is a common phenomenon in tumor cells.[82].. Antibodies are often produced against tumor cellsComplement systemIs also attempted to destroy those cells[78].

Obviously, some tumors escape the immune system and go to cancer.[83].. Tumor cells often express low numbers of MHC class I molecules on their surface, thus avoiding detection by cytotoxic T cells (CTLs).[81].. In addition, some tumor cells release products that inhibit the immune response, such as cytokines.TGF-βWhen secretingMacrophageAnd lymphocyte activity is suppressed[84].. In addition to tumor cellsImmune toleranceMay develop and prevent the immune system from attacking tumor cells anymore[83].

Paradoxically, tumor cells lure macrophagesCytokineAnd macrophages with cytokines that then allow tumor cells to growGrowth factorsMacrophages can promote tumor growth when they produce[85].. In addition in tumor cellsHypoxiaTumor cells combine state and macrophage-producing cytokinesTransitionIt reduces the production of proteins that block the cancer and helps the cancer cells spread.

Physiological control

hormoneActs as an immunomodulator and may be able to alter the sensitivity of the immune system. For example, for womenSex hormoneAlso for adaptive immune responses[86] Also for the innate immune response[87] It is known to have immunostimulatory activity.Systemic lupus erythematosuslikeAutoimmune diseaseSelectively attacks women, but often onsetpubertyThere is a coincidence of time that it is. In contrasttestosteronelikeMale hormoneSeems to have immunosuppressive power[88].. Some other hormones appear to control the immune system, the most famous of which.Prolactin,Growth hormone,Vitamin DIs[89][90].. Hormone levels continue to decline over the years, causing a diminished immune response, especially for older people[91].. On the contrary, some hormones are controlled by the immune system, and as a prominent one,Thyroid hormoneIs controlled by the immune system[92].

The immune systemSleep,休息Enhanced by[93] stressDamaged by[94].

dietMay affect the immune system. For example freshfruit,Vegetables, Some kindfatty acidRich infood TheHealthMaintains and promotes the immune system[95].. In the same wayFetusUndernutrition can cause lifelong damage to the immune system[96]. traditionalMedical scienceThen.HerbsIt is believed that some of them stimulate the immune system. For such herbs, for exampleEchinacea,Licorice,Talus(Bead),Salvia,garlic,America·ElderberryFruit,Shiitake mushroom,Hyssop, And moreHoneyThere is. Studies suggest that such herbs stimulate the immune system, even though they act complexly and are difficult to characterize.[97].

Manipulation in medicine

The immune response is autoimmunity,Allergies, TransplantRejectionTo suppress the unwanted response that results from, and also largely escape the immune systemPathogenIt can be manipulated to stimulate the defense response against.vaccineInoculation andSerum therapyOf the immune systemAntigen-antibody reactionIs used.Immunosuppressive drug TheAutoimmune diseaseOr excessive組織Destruction is happeningInflammationUsed to control transplantation and to prevent transplant rejection after organ transplantation[26][98].

Anti-inflammatory drugIs often used to control the effects of inflammation.GlucocorticoidIs the most powerful of these chemicals. But these drugs have many unexpectedSide effectsCan have (eg, centrality)obesity,Hyperglycemia,osteoporosis). Use must be tightly controlled[99].. Therefore, use small amounts of anti-inflammatory drugsMethotrexate,AzathioprineIt is often used in combination with cytotoxic or immunosuppressive drugs such as. Cytotoxic drugs activateT cellsInhibits an immune response that kills dividing cells such as. However, since the killing action is indistinguishable, the cells that are constantly dividing and theirorganIs affected and this istoxicityBrings side effects[98].CyclosporineImmunosuppressive drugs such as block the signal transduction system and thus prevent T cells from responding correctly to the signal.[100].

Larger drugs (> 500Da) may neutralize the immune response, especially when given repeatedly and in large doses.bigpeptideandproteinThe effectiveness of chemicals based on (typically over 6,000 Da) is limited. The drug itself is not immunogenic and may be co-administered with immunogenic substances. Such a thingTaxolI sometimes see it. To predict the immunogenicity of peptides and proteinsComputerMethods have been developed, especially for treatmentantibodyDesign, potential toxicity to viral coat particlesmutationIt is useful for evaluating and verifying peptide-based drug treatment. Mainly in early techniquesEpitopeIn the areaHydrophilic Ofamino acid HydrophobicI relied on the observation that it was overexpressed than the amino acids in[101]In more recent research, computers are usually based on well-studied viral proteins, using it as a learning material for known epitopes.DatabaseRelies on computer-learned techniques for[102].. A publicly accessible database has been established for cataloging epitopes known to be recognized by B cells.[103].. ImmunogenicBioinformaticsThe field of study based on is newly born and is referred to as immunoinformatics.[104].

Manipulation of pathogens

PathogenSuccess depends on the ability of the host to escape the immune response. Therefore the pathogen works well for the hostinfectionWe have developed some methods that can be done while avoiding immune-mediated destruction.[105].. Bacteria often secrete it for physical barriers酵素digestionGet through by doing. For example, the use of the type II secretory system.[106].. AlternativelyType III secretion systemIs used to insert a tube that punctures the host cell. From pathogen to host directly through this tubeproteinTo move. Proteins transported through tubes are often used to stop host defense[107].

The avoidance strategy used by some pathogens to escape the natural immune system is intracellular replication (also called intracellular pathogenicity). In this case, the pathogen spends most of its life history in the host cell. There, immune cells,antibody,in additioncomplementIt is protected from them without direct contact with them. An example of an intracellular pathogenウ イ ル ス,Food poisoningBacterialSalmonella,Eukaryote OfParasiteIsmalariaWhat causesPlasmodium falciparum) AndLeishmaniasisWhat causesLeishmania spp.) and so on.Mycobacterium tuberculosis(Mycobacterium tuberculosis) Survives in protective capsules that block complement lysis[108].. Many pathogens secrete chemicals that weaken the host's immune response and misdirect[105].. Some bacteria are biological to protect against cells and proteins of the immune systemthe filmThere is something that forms. Such biological films are found in many successful infections, such asCystic fibrosisChronicPseudomonas aeruginosaInfection or(English editionHave an infection[109].. There are other bacteria that express surface proteins that bind to antibodies and reduce the efficacy of the antibodies. In this exampleStreptococcus(G protein),Staphylococcus aureus(),(English editionThere is ()[110].

The mechanism by which the virus escapes the adaptive immune system is more complicated. Easy way is essentialEpitopeIs to rapidly change epitopes on the surface of the virus that are hidden and completely non-essential (amino acids and / or sugars). For exampleHIVIs constantly a protein in the outer membrane of the virus that is essential for invading the host's target cellsmutationWake up. These frequent changes in antigens target these proteinsvaccineWill explain that you are failing. Masking antigens with host molecules is a common strategy for escaping host cells.[111].. In HIV, the outer membrane that covers the virus is made from the outermost membrane of the host cell. These "self-covering" viruses make it difficult for the immune system to recognize them as "non-self."[112].

Immunology and its history

ImmunologyIs a science that studies the structure and function of the immune system.

This was born out of medicine and early research was about the cause of immunity to disease. As far as we know, immunity was first mentioned.BC430 OfAthensDuring the epidemic.ThucydidesWrote that people who have previously recovered from their illness will not be affected twice by caring for their patients.[113].. The acquired immunity observed in this way was later explored by Louis Pasteur, leading to the development of vaccination and the proposal of microbial etiology of the disease.[114].. Pasteur's theory confronts the theory that was prevailing at the time of illness, and this proof was made in 1891.Robert KochKoch won the Nobel Prize in 1905, although he had to wait until it was proved that the microbes made by him were the cause of the infection.[115].. In 1901(English editionby,yellow feverWhen the virus was discovered, the virus was confirmed as[116].

Immunology has made great strides towards the end of the 19th century, but in the midst of rapid development the study of humoral and cell-mediated immunity[117] Of particular importancePaul EhrlichIn his work, he explained the specificity of the antigen-antibody reaction.Side chain theoryWas chanted.Humoral immunityContribution to understanding of cell-mediated immunity researchIlya MetynikovRecognized for receiving the 1908 Nobel Prize in collaboration with[118].

Footnote/Source

[How to use footnotes]
  1. ^ a b c Beck, Gregory; Gail S. Habicht (November 1996). “Immunity and the Invertebrates” (PDF). Scientific American: 60--66. http://www.scs.carleton.ca/~soma/biosec/readings/sharkimmu-sciam-Nov1996.pdf 2007/1/1Browse.. 
  2. ^ Smith AD (Ed) Oxford dictionary of biochemistry and molecular biology. (1997) Oxford University Press. ISBN-0 19-854768-4
  3. ^ a b c d e f g h i Alberts, Bruce; Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walters (2002). Molecular Biology of the Cell; Fourth Edition. New York and London: Garland Science. ISBN-0 8153-3218-1. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=mboc4.TOC&depth=2 
  4. ^ a b Litman G, Cannon J, Dishaw L (2005). “Reconstructing immune phylogeny: new perspectives”. Nat Rev Immunol 5 (11): 866--79. two:10.1038 / nri1712. PMID 16261174. 
  5. ^ a b c Mayer, Gene (2006). “Immunology --Chapter One: Innate (non-specific) Immunity". Microbiology and Immunology On-Line Textbook. USC School of Medicine. 2007/1/1Browse.
  6. ^ Boyton R, Openshaw P (2002). “Pulmonary defenses to acute respiratory infection”. Br Med Bull 61: 1--12. two:10.1093 / bmb / 61.1.1. PMID 11997295. 
  7. ^ Agerberth B, Gudmundsson G. “Host antimicrobial defense peptides in human disease”. Curr Top Microbiol Immunol 306: 67--90. two:10.1007 / 3-540-29916-5_3. PMID 16909918. 
  8. ^ Moreau J, Girgis D, Hume E, Dajcs J, Austin M, O'Callaghan R (2001). “Phospholipase A (2) in rabbit tears: a host defense against Staphylococcus aureus”. Invest Ophthalmol Vis Sci 42 (10): 2347--54. PMID 11527949. http://www.iovs.org/cgi/content/full/42/10/2347. 
  9. ^ Hankiewicz J, Swierczek E (1974). “Lysozyme in human body fluids”. Clin Chim Acta 57 (3): 205--9. two:10.1016 / 0009-8981 (74) 90398-2. PMID 4434640. 
  10. ^ Fair W, Couch J, Wehner N (1976). “Prostatic antibacterial factor. Identity and significance”. Urology 7 (2): 169--77. two:10.1016 / 0090-4295 (76) 90305-8. PMID 54972. 
  11. ^ Yenugu S, Hamil K, Birse C, Ruben S, French F, Hall S (2003). “Antibacterial properties of the sperm-binding proteins and peptides of human epididymis 2 (HE2) family; salt sensitivity, structural dependence and their interaction with outer and cytoplasmic membranes of Escherichia coli”. Biochem J 372 (Pt 2): 473--83. two:10.1042 / BJ20030225. PMID 12628001. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1223422&blobtype=pdf. 
  12. ^ Gorbach S (1990). “Lactic acid bacteria and human health”. Ann Med 22 (1): 37--41. two:10.3109/07853899009147239. PMID 2109988. 
  13. ^ Reid G, Bruce A (2003). “Urogenital infections in women: can probiotics help?”. Postgrad Med J 79 (934): 428--32. two:10.1136 / pmj.79.934.428. PMID 12954951. http://pmj.bmj.com/cgi/content/full/79/934/428. 
  14. ^ Salminen S, Gueimonde M, Isolauri E (2005). “Probiotics that modify disease risk”. J Nutr 135 (5): 1294--8. PMID 15867327. http://jn.nutrition.org/cgi/content/full/135/5/1294. 
  15. ^ Reid G, Jass J, Sebulsky M, McCormick J (2003). “Potential uses of probiotics in clinical practice”. Clin Microbiol Rev 16 (4): 658--72. two:10.1128 / CMR.16.4.658-672.2003. PMID 14557292. 
  16. ^ Hill L, Embil J (1986). “Vaginitis: current microbiologic and clinical concepts”. CMAJ 134 (4): 321--31. PMID 3510698. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1490817&blobtype=pdf. 
  17. ^ Medzhitov R (2007). “Recognition of microorganisms and activation of the immune response”. Nature 449 (7164): 819--26. two:10.1038 / nature06246. PMID 17943118. 
  18. ^ Matzinger P (2002). “The danger model: a renewed sense of self”. Science 296 (5566): 301-5. two:10.1126 / science.1071059. 
  19. ^ Kawai T, Akira S (2006). “Innate immune recognition of viral infection”. Nat Immunol 7 (2): 131--7. two:10.1038 / ni1303. PMID 16424890. 
  20. ^ Miller, SB (2006). “Prostaglandins in Health and Disease: An Overview”. Seminars in Arthritis and Rheumatism 36 (1): 37--49. two:10.1016 / j.semarthrit.2006.03.005. PMID 16887467. 
  21. ^ Ogawa Y, Calhoun WJ. (2006). “The role of leukotrienes in airway inflammation”. J Allergy Clin Immunol. 118 (4): 789--98. two:10.1016 / j.jaci.2006.08.009. PMID 17030228. 
  22. ^ Le Y, Zhou Y, Iribarren P, Wang J (2004). “Chemokines and chemokine receptors: their manifold roles in homeostasis and disease”. Cell Mol Immunol 1 (2): 95--104. PMID 16212895. http://www.nature.com/bjp/journal/v147/n1s/pdf/0706475a.pdf. 
  23. ^ Martin P, Leibovich S (2005). “Inflammatory cells during wound repair: the good, the bad and the ugly”. Trends Cell Biol 15 (11): 599--607. two:10.1016 / j.tcb.2005.09.002. PMID 16202600. 
  24. ^ a b Rus H, Cudrici C, Niculescu F (2005). “The role of the complement system in innate immunity”. Immunol Res 33 (2): 103--12. two:10.1385 / IR: 33: 2: 103. PMID 16234578. 
  25. ^ Mayer, Gene (2006). “Immunology --Chapter Two: Complement". Microbiology and Immunology On-Line Textbook. USC School of Medicine. 2007/1/1Browse.
  26. ^ a b c d e f Janeway CA, Jr. et al (2005). Immunobiology. (6th ed. Ed.). Garland Science. ISBN-0 443-07310-4 
  27. ^ Liszewski M, Farries T, Lublin D, Rooney I, Atkinson J (1996). “Control of the complement system”. Adv Immunol 61: 201--83. two:10.1016 / S0065-2776 (08) 60868-8. PMID 8834497. 
  28. ^ Sim R, Tsiftsoglou S (2004). “Proteases of the complement system”. Biochem Soc Trans 32 (Pt 1): 21--7. two:10.1042 / BST0320021. PMID 14748705. http://www.biochemsoctrans.org/bst/032/0021/0320021.pdf. 
  29. ^ Ryter A (1985). “Relationship between ultrastructure and specific functions of macrophages”. Comp Immunol Microbiol Infect Dis 8 (2): 119--33. two:10.1016 / 0147-9571 (85) 90039-6. PMID 3910340. 
  30. ^ Langermans J, Hazenbos W, van Furth R (1994). “Antimicrobial functions of mononuclear phagocytes”. J Immunol Methods 174 (1--2): 185--94. two:10.1016 / 0022-1759 (94) 90021-3. PMID 8083520. 
  31. ^ May R, Machesky L (2001). “Phagocytosis and the actin cytoskeleton”. J Cell Sci 114 (Pt 6): 1061--77. PMID 11228151. http://jcs.biologists.org/cgi/reprint/114/6/1061. 
  32. ^ Salzet M, Tasiemski A, Cooper E (2006). “Innate immunity in lophotrochozoans: the annelids”. Curr Pharm Des 12 (24): 3043--50. two:10.2174/138161206777947551. PMID 16918433. 
  33. ^ Zen K, Parkos C (2003). “Leukocyte-epithelial interactions”. Curr Opin Cell Biol 15 (5): 557--64. two:10.1016 / S0955-0674 (03) 00103-0. PMID 14519390. 
  34. ^ a b Stvrtinova', Viera; Ja'n Jakubovsky' and Ivan Huli'n (1995). Inflammation and Fever from Pathophysiology: Principles of Disease. Computing Center, Slovak Academy of Sciences: Academic Electronic Press. オ リ ジ ナ ルArchived as of October 2001, 7.. https://web.archive.org/web/20010711220523/http://nic.savba.sk/logos/books/scientific/Inffever.html 2007/1/1Browse. 
  35. ^ Bowers, William (2006). “Immunology -Chapter Thirteen: Immunoregulation". Microbiology and Immunology On-Line Textbook. USC School of Medicine. 2007/1/4Browse.
  36. ^ a b Guermonprez P, Valladeau J, Zitvogel L, The'ry C, Amigorena S (2002). “Antigen presentation and T cell stimulation by dendritic cells”. Annu Rev Immunol 20: 621--67. two:10.1146 / annurev.immunol.20.100301.064828. PMID 11861614. 
  37. ^ Middleton D, Curran M, Maxwell L (2002). “Natural killer cells and their receptors”. Transpl Immunol 10 (2--3): 147--64. two:10.1016 / S0966-3274 (02) 00062-X. PMID 12216946. 
  38. ^ Kariyawasam H, Robinson D (2006). “The eosinophil: the cell and its weapons, the cytokines, its locations”. Semin Respir Crit Care Med 27 (2): 117--27. two:10.1055 / s-2006-939514. PMID 16612762. 
  39. ^ Krishnaswamy G, Ajitawi O, Chi D. “The human mast cell: an overview”. Methods Mol Biol 315: 13--34. PMID 16110146. 
  40. ^ Pancer Z, Cooper M (2006). “The evolution of adaptive immunity”. Annu Rev Immunol 24: 497--518. two:10.1146 / annurev.immunol.24.021605.090542. PMID 16551257. 
  41. ^ Holtmeier W, Kabelitz D. “Gammadelta T cells link innate and adaptive immune responses”. Chem Immunol Allergy 86: 151-83. PMID 15976493. 
  42. ^ a b "Understanding the Immune System: How it Works (PDF) ”. (NIAID). As of January 2007, 1オ リ ジ ナ ル[Broken link]More archives.2007/1/1Browse.
  43. ^ Harty J, Tvinnereim A, White D (2000). “CD8 + T cell effector mechanisms in resistance to infection”. Annu Rev Immunol 18: 275-308. two:10.1146 / annurev.immunol.18.1.275. PMID 10837060. 
  44. ^ a b Radoja S, Frey A, Vukmanovic S (2006). “T-cell receptor signaling events triggering granule exocytosis”. Crit Rev Immunol 26 (3): 265-90. PMID 16928189. 
  45. ^ Abbas A, Murphy K, Sher A (1996). “Functional diversity of helper T lymphocytes”. Nature 383 (6603): 787-93. two:10.1038 / 383787a0. PMID 8893001. 
  46. ^ McHeyzer-Williams L, Malherbe L, McHeyzer-Williams M (2006). “Helper T cell-regulated B cell immunity”. Curr Top Microbiol Immunol 311: 59-83. two:10.1007 / 3-540-32636-7_3. PMID 17048705. 
  47. ^ Kovacs B, Maus M, Riley J, Derimanov G, Koretzky G, June C, Finkel T (2002). “Human CD8 + T cells do not require the polarization of lipid rafts for activation and proliferation”. Proc Natl Acad Sci US a 99 (23): 15006--11. two:10.1073 / pnas.232058599. PMID 12419850. http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=12419850&cmd=showdetailview. 
  48. ^ Grewal I, Flavell R (1998). “CD40 and CD154 in cell-mediated immunity”. Annu Rev Immunol 16: 111-35. two:10.1146 / annurev.immunol.16.1.111. PMID 9597126. 
  49. ^ Girardi M (2006). “Immunosurveillance and immunoregulation by γδ T cells”. J Invest Dermatol 126 (1): 25--31. two:10.1038 / sj.jid.5700003. PMID 16417214. 
  50. ^ Holtmeier W, Kabelitz D (2005). “Γδ T cells link innate and adaptive immune responses”. Chem Immunol Allergy 86: 151--183. two:10.1159/000086659. PMID 15976493. 
  51. ^ a b Sproul T, Cheng P, Dykstra M, Pierce S (2000). “A role for MHC class II antigen processing in B cell development”. Int Rev Immunol 19 (2--3): 139--55. two:10.3109/08830180009088502. PMID 10763706. 
  52. ^ Kehry M, Hodgkin P (1994). “B-cell activation by helper T-cell membranes”. Crit Rev Immunol 14 (3--4): 221--38. PMID 7538767. 
  53. ^ Bowers, William (2006). “Immunology --Chapter nine: Cells involved in immune responses". Microbiology and Immunology On-Line Textbook. USC School of Medicine. 2007/1/4Browse.
  54. ^ MN Alder, IB Rogozin, LM Iyer, GV Glazko, MD Cooper, Z. Pancer (2005). “Diversity and Function of Adaptive Immune Receptors in a Jawless Vertebrate”. Science 310 (5756): 1970--1973. two:10.1126 / science.1119420. PMID 16373579. 
  55. ^ Saji F, Samejima Y, Kamiura S, Koyama M (1999). “Dynamics of immunoglobulins at the feto-maternal interface”. Rev Reprod 4 (2): 81--9. two:10.1530 / ror.0.0040081. PMID 10357095. http://ror.reproduction-online.org/cgi/reprint/4/2/81.pdf. 
  56. ^ Van de Perre P (2003). “Transfer of antibody via mother's milk”. Vaccine 21 (24): 3374--6. two:10.1016 / S0264-410X (03) 00336-0. PMID 12850343. 
  57. ^ Keller, Margaret A. and E. Richard Stiehm (2000). “Passive Immunity in Prevention and Treatment of Infectious Diseases”. Clinical Microbiology Reviews 13 (4): 602--614. two:10.1128 / CMR.13.4.602-614.2000. PMID 11023960. http://cmr.asm.org/cgi/content/full/13/4/602. 
  58. ^ Death and DALY estimates for 2002 by cause for WHO Member States. World Health Organization.Retrieved on.
  59. ^ Singh M, O'Hagan D (1999). “Advances in vaccine adjuvants”. Nat Biotechnol 17 (11): 1075--81. two:10.1038/15058. PMID 10545912. 
  60. ^ Aw D, Silva A, Palmer D (2007). “Immunosenescence: emerging challenges for an aging population”. Immunology 120 (4): 435--446. two:10.1111 / j.1365-2567.2007.02555.x. PMID 17313487. 
  61. ^ a b c d Chandra, RK (1997). “Nutrition and the immune system: an introduction”. American Journal of Clinical Nutrition Vol 66: 460S--463S. PMID 9250133. http://www.ajcn.org/cgi/content/abstract/66/2/460S.  Free full-text pdf available
  62. ^ Miller JF (2002). “The discovery of thymus function and of thymus-derived lymphocytes”. Immunol. Rev. 185: 7--14. PMID 12190917. http://www.blackwell-synergy.com/doi/abs/10.1034/j.1600-065X.2002.18502.x. 
  63. ^ Joos L, Tamm M (2005). “Breakdown of pulmonary host defense in the immunocompromised host: cancer chemotherapy”. Proc Am Thorac Soc 2 (5): 445--8. two:10.1513 / pats.200508-097JS. PMID 16322598. http://pats.atsjournals.org/cgi/content/full/2/5/445. 
  64. ^ Copeland K, Heeney J (1996). “T helper cell activation and human retroviral pathogenesis”. Microbiol Rev 60 (4): 722--42. PMID 8987361. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=239461&blobtype=pdf. 
  65. ^ Miller J (1993). “Self-nonself discrimination and tolerance in T and B lymphocytes”. Immunol Res 12 (2): 115--30. two:10.1007 / BF02918299. PMID 8254222. 
  66. ^ a b c d Ghaffar, Abdul (2006). “Immunology --Chapter Seventeen: Hypersensitivity Reactions". Microbiology and Immunology On-Line Textbook. USC School of Medicine. 2007/1/1Browse.
  67. ^ Bickle T, Kru "ger D (1993). “Biology of DNA restriction”. Microbiol Rev 57 (2): 434--50. PMID 8336674. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=372918&blobtype=pdf. 
  68. ^ Barrangou R, Fremaux C, Deveau H, et al (March 2007). “CRISPR provides acquired resistance against viruses in prokaryotes”. Science (journal) 315 (5819): 1709--12. two:10.1126 / science.1138140. PMID 17379808. 
  69. ^ Brouns SJ, Jore MM, Lundgren M, et al (August 2008). “Small CRISPR RNAs guide antiviral defense in prokaryotes”. Science (journal) 321 (5891): 960--4. two:10.1126 / science.1159689. PMID 18703739. 
  70. ^ Stram Y, Kuzntzova L. (2006). “Inhibition of viruses by RNA interference”. Virus Genes 32 (3): 299--306. two:10.1007 / s11262-005-6914-0. PMID 16732482. 
  71. ^ a b Schneider, David (Spring 2005). “Innate Immunity --Lecture 4: Plant immune responses”. Stanford University Department of Microbiology and Immunology. As of June 2007, 6オ リ ジ ナ ル[Broken link]More archives.2007/1/1Browse.
  72. ^ Baulcombe D (2004). “RNA silencing in plants”. Nature 431 (7006): 356--63. two:10.1038 / nature02874. PMID 15372043. 
  73. ^ Morgan R et al(2006). “Cancer regression in patients after transfer of genetically engineered lymphocytes”. Science 314: 126--129. two:10.1126 / science.1129003. PMID 16946036. 
  74. ^ a b Andersen MH, Schrama D, Thor Straten P, Becker JC (2006). “Cytotoxic T cells”. J Invest Dermatol 126 (1): 32--41. two:10.1038 / sj.jid.5700001. PMID 16417215. 
  75. ^ Boon T, van der Bruggen P (1996). “Human tumor antigens recognized by T lymphocytes”. J Exp Med 183: 725--29. two:10.1084 / jem.183.3.725. PMID 8642276. 
  76. ^ Castelli C, Rivoltini L, Andreola G, Carrabba M, Renkvist N, Parmiani G (2000). “T cell recognition of melanoma-associated antigens”. J Cell Physiol 182: 323--31. two:10.1002/(SICI)1097-4652(200003)182:3<323::AID-JCP2>3.0.CO;2-#. PMID 10653598. 
  77. ^ a b Romero P, Cerottini JC, Speiser DE (2006). “The human T cell response to melanoma antigens”. Adv Immunol. 92: 187--224. two:10.1016 / S0065-2776 (06) 92005-7. PMID 17145305. 
  78. ^ a b Guevara-Patino JA, Turk MJ, Wolchok JD, Houghton AN (2003). “Immunity to cancer through immune recognition of altered self: studies with melanoma”. Adv Cancer Res. 90: 157--77. two:10.1016 / S0065-230X (03) 90005-4. PMID 14710950. 
  79. ^ Renkvist N, Castelli C, Robbins PF, Parmiani G (2001). “A listing of human tumor antigens recognized by T cells”. Cancer Immunol Immunother 50: 3--15. two:10.1007 / s002620000169. PMID 11315507. 
  80. ^ Gerloni M, Zanetti M. (2005). “CD4 T cells in tumor immunity”. .Springer Semin Immunopathol 27 (1): 37--48. two:10.1007 / s00281-004-0193-z. PMID 15965712. 
  81. ^ a b Seliger B, Ritz U, Ferrone S (2006). “Molecular mechanisms of HLA class I antigen abnormalities following viral infection and transformation”. Int J Cancer 118 (1): 129--38. two:10.1002 / ijc.21312. PMID 16003759. 
  82. ^ Hayakawa Y, Smyth MJ. (2006). “Innate immune recognition and suppression of tumors”. Adv Cancer Res 95: 293--322. two:10.1016 / S0065-230X (06) 95008-8. PMID 16860661. 
  83. ^ a b Seliger B (2005). “Strategies of tumor immune evasion”. BioDrugs 19 (6): 347--54. two:10.2165 / 00063030-200519060-00002. PMID 16392887. 
  84. ^ Frumento G, Piazza T, Di Carlo E, Ferrini S (2006). “Targeting tumor-related immunosuppression for cancer immunotherapy”. Endocr Metab Immune Disord Drug Targets 6 (3): 233--7. two:10.2174/187153006778250019. PMID 17017974. 
  85. ^ Stix, Gary (July 2007). “A Malignant Flame” (PDF). Scientific American: 60--67. オ リ ジ ナ ルArchived as of October 2011, 7.. https://web.archive.org/web/20110716015048/http://podcast.sciam.com/daily/pdf/sa_d_podcast_070619.pdf 2007/1/1Browse.. 
  86. ^ Wira, CR; Crane-Godreau M, Grant K (2004). “Endocrine regulation of the mucosal immune system in the female reproductive tract”. In In: Ogra PL, Mestecky J, Lamm ME, Strober W, McGhee JR, Bienenstock J (eds.). Mucosal Immunology. San Francisco: Elsevier. ISBN 0124915434 
  87. ^ Lang, TJ (2004). “Estrogen as an immunomodulator”. Clin Immunol 113: 224–230. two:10.1016 / j.clim.2004.05.011. PMID 15507385. 
    Moriyama, A; Shimoya K, Ogata I et al. (1999). “Secretory leukocyte protease inhibitor (SLPI) concentrations in cervical mucus of women with normal menstrual cycle”. Molecular Human Reproduction 5: 656–661. two:10.1093 / molehr / 5.7.656. PMID 10381821. http://molehr.oxfordjournals.org/cgi/content/full/5/7/656. 
    Cutolo, M; Sulli A, Capellino S, Villaggio B, Montagna P, Seriolo B, Straub RH (2004). “Sex hormones influence on the immune system: basic and clinical aspects in autoimmunity”. Lupus 13: 635–638. two:10.1191 / 0961203304lu1094oa. PMID 15485092. 
    King, AE; Critchley HOD, Kelly RW (2000). “Presence of secretory leukocyte protease inhibitor in human endometrium and first trimester decidua suggests an antibacterial role”. Molecular Human Reproduction 6: 191–196. two:10.1093 / molehr / 6.2.191. PMID 10655462. http://molehr.oxfordjournals.org/cgi/content/full/6/2/191. 
  88. ^ Fimmel; Zouboulis CC (2005). “Influence of physiological androgen levels on wound healing and immune status in men”. Aging Male 8: 166–174. two:10.1080/13685530500233847. PMID 16390741. 
  89. ^ Dorshkind, K; Horseman ND (2000). “The Roles of Prolactin, Growth Hormone, Insulin-Like Growth Factor-I, and Thyroid Hormones in Lymphocyte Development and Function: Insights from Genetic Models of Hormones and Hormone Receptor Deficiency”. Endocrine Reviews 21: 292–312. two:10.1210 / er.21.3.292. PMID 10857555. http://edrv.endojournals.org/cgi/content/full/21/3/292?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=Dorshkind%2C+K%3B+Horseman+ND+&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT. 
  90. ^ Nagpal, Sunil; Songqing Naand and Radhakrishnan Rathnachalam (2005). “Noncalcemic Actions of Vitamin D Receptor Ligands”. Endocrine Reviews 26 (5): 662–687. two:10.1210 / er.2004-0002. PMID 15798098. http://edrv.endojournals.org/cgi/content/full/26/5/662. .
  91. ^ Hertoghe, T (2005). “The“ multiple hormone deficiency ”theory of aging: Is human senescence caused mainly by multiple hormone deficiencies?”. Annals of the New York Academy of Science 1051: 448–465. two:10.1196 / annals.1322.035. PMID 16399912. 
  92. ^ Klein, JR (2006). “The immune system as a regulator of thyroid hormone activity”. Exp Biol Med 231: 229–236. PMID 16514168. 
  93. ^ Lange, T; Perras B, Fehm HL, Born J (2003). “Sleep Enhances the Human Antibody response to Hepatitis A Vaccination”. Psychosomatic Medicine 65: 831–835. two:10.1097 / 01.PSY.0000091382.61178.F1. PMID 14508028. http://www.psychosomaticmedicine.org/cgi/content/full/65/5/831. 
  94. ^ Khansari, DN; Murgo AJ, Faith RE (1990). “Effects of stress on the immune system”. Immunology Today 11: 170–175. two:10.1016 / 0167-5699 (90) 90069-L. PMID 2186751. 
  95. ^ Pond, CM (2005). “Adipose tissue and the immune system”. Prostaglandins, Leukotrienes, and Essential Fatty Acids 73: 17--30. two:10.1016 / j.plefa.2005.04.005. PMID 15946832. 
  96. ^ Langley-Evans, SC; Carrington LJ (2006). “Diet and the developing immune system”. Lupus 15: 746–752. two:10.1177/0961203306070001. PMID 17153845. 
  97. ^ Spelman, K; Burns J, Nichols D, Winters N, Ottersberg S, Tenborg M (2006). “Modulation of cytokine expression by traditional medicines: a review of herbal immunomodulators”. Alternative Medicine reviews 11: 128–150. PMID 16813462. 
    Brush, J; Mendenhall E, Guggenheim A, Chan T, Connelly E, Soumyanth A, Buresh R, Barrett R, Zwickey H (2006). “The effect of Echinacea purpurea, Astragalus membranaceus and Glycyrrhiza glabra on CD69 expression and immune cell activation in humans ”. Phytotherapy Research 20: 687–695. two:10.1002 / ptr.1938. PMID 16807880. 
  98. ^ a b Taylor A, Watson C, Bradley J (2005). “Immunosuppressive agents in solid organ transplantation: Mechanisms of action and therapeutic efficacy”. Crit Rev Oncol Hematol 56 (1): 23--46. two:10.1016 / j.critrevonc.2005.03.012. PMID 16039869. 
  99. ^ Barnes P (2006). “Corticosteroids: the drugs to beat”. Eur J Pharmacol 533 (1--3): 2--14. two:10.1016 / j.ejphar.2005.12.052. PMID 16436275. 
  100. ^ Masri M (2003). “The mosaic of immunosuppressive drugs”. Mol Immunol 39 (17--18): 1073--7. two:10.1016 / S0161-5890 (03) 00075-0. PMID 12835079. 
  101. ^ Welling GW, Wiejer WJ, van der Zee R, Welling-Werster S. (1985). “Prediction of sequential antigenic regions in proteins”. J Mol Recognit 88 (2): 215--8. PMID 2411595. 
  102. ^ Sollner J, Mayer B. (2006). “Machine learning approaches for prediction of linear B-cell epitopes on proteins”. Journal of Molecular Recognition 19 (3): 200--8. two:10.1002 / jmr.771. PMID 16598694. 
  103. ^ Saha S, Bhasin M, Raghava GP. (2005). “Bcipep: a database of B-cell epitopes”. BMC Bioinformatics 6 (1): 79. two:10.1186 / 1471-2105-6-79. PMID 15921533. 
  104. ^ Flower DR, Doytchinova IA. (2002). “Immunoinformatics and the prediction of immunogenicity”. Appl Bioinformatics 1 (4): 167--76. PMID 15130835. 
  105. ^ a b Finlay B, McFadden G (2006). “Anti-immunology: evasion of the host immune system by bacterial and viral pathogens”. Cell 124 (4): 767--82. two:10.1016 / j.cell.2006.01.034. PMID 16497587. 
  106. ^ Cianciotto NP. (2005). “Type II secretion: a protein secretion system for all seasons”. Trends Microbiol. 13 (12): 581--8. two:10.1016 / j.tim.2005.09.005. PMID 16216510. 
  107. ^ Winstanley C, Hart CA (2001). “Type III secretion systems and pathogenicity islands”. J Med Microbiol. 50 (2): 116--26. PMID 11211218. 
  108. ^ Finlay B, Falkow S (1997). “Common themes in microbial pathogenicity revisited”. Microbiol Mol Biol Rev 61 (2): 136--69. PMID 9184008. http://mmbr.asm.org/cgi/reprint/61/2/136.pdf. 
  109. ^ Kobayashi H (2005). “Airway biofilms: implications for pathogenesis and therapy of respiratory tract infections”. Treat Respir Med 4 (4): 241--53. two:10.2165 / 00151829-200504040-00003. PMID 16086598. 
  110. ^ Housden N, Harrison S, Roberts S, Beckingham J, Graille M, Stura E, Gore M (2003). “Immunoglobulin-binding domains: Protein L from Peptostreptococcus magnus”. Biochem Soc Trans 31 (Pt 3): 716--8. two:10.1042 / BST0310716. PMID 12773190. http://www.biochemsoctrans.org/bst/031/0716/0310716.pdf. 
  111. ^ Burton, Dennis R .; Robyn L. Stanfield and Ian A. Wilson (2005). “Antibody vs. HIV in a clash of evolutionary titans”. Proc Natl Acad Sci US A. 102 (42): 14943--8. two:10.1073 / pnas.0505126102. PMID 16219699. 
  112. ^ Cantin R, Methot S, Tremblay MJ. (2005). “Plunder and stowaways: incorporation of cellular proteins by enveloped viruses”. J Virol. 79 (11): 6577-87. two:10.1128 / JVI.79.11.6577-6587.2005. PMID 15890896. 
  113. ^ Retief F, Cilliers L (1998). “The epidemic of Athens, 430-426 BC”. S Afr Med J 88 (1): 50--3. PMID 9539938. 
  114. ^ Plotkin S (2005). “Vaccines: past, present and future”. Nat Med 11 (4 Suppl): S5--11. two:10.1038 / nm1209. PMID 15812490. 
  115. ^ The Nobel Prize in Physiology or Medicine 1905 Nobelprize.org Accessed January 8 2007.
  116. ^ Major Walter Reed, Medical Corps, US Army Archived August 2007, 10, at the Wayback Machine. Walter Reed Army Medical Center. Accessed January 8 2007.
  117. ^ Translated by FG ​​Binnie. (1905) (Full Text Version: Google Books). Immunity in Infective Diseases.Cambridge University Press. http://books.google.com/books?vid=OCLC03666307&id=ywKp9YhK5t0C&printsec=titlepage&vq=Ehrlich&dq=history+of+humoral+immunity 
  118. ^ The Nobel Prize in Physiology or Medicine 1908 Nobelprize.org Accessed January 8 2007

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