自身防御机制.ppt

MECHANISMSOFSELF DEFENSE Part1 CharlotteA Richmond PhD RN INNATEDEFENSES Body s1stlineofdefense anatomicbarriersTheskin mucousmembranesIfthesedefensesarepenetrated Mechanicalclearance2ndlineofdefense Inflammatoryresponse IMMUNERESPONSE 3rdLineofdefense ImmuneResponseSlower specificcomparedtoinflammatoryresponseInflammatory immuneresponsescomplementeachother interactincomplexways THEIMMUNESYSTEM ExtraordinarycomplexsystemElaborate dynamiccommunicationnetworkRecognizes respondstoantigens Cells moleculesoftheimmunesystemprotectthenosefromattackbyavirus CHARACTERISTICSOFIMMUNERESPONSE ImmunityStateofprotection primarilyagainstinfectionsCharacterizedbymemory specificityAntigensChemicalsubstancesthatreactwithpreformedcomponentsoftheimmuneresponseImmunogensAntigensthatinduceanimmuneresponseHaptensAntigensmustbeboundtocarrierstoinduceanimmuneresponse Self AntigensAntigensonhostcellsNotrecognizedasimmunogenicbyhost simmunesystemAconditioncalledtolerance CHARACTERISTICSOFIMMUNERESPONSE INDUCTIONOFIMMUNERESPONSE MostimmunesystemcellsareWBCsImmunocytes lymphocytes are1typeofWBC2majorclassesofimmunocytesTlymphocytes Tcells Blymphocytes Bcells ImmuneresponseischaracterizedbytheactivationofBcells Tcells BCELLS Developsfromastemcellthatmaturesunderhormonalcontrolinbursal equivalenttissues bonemarrow DevelopsintoamatureplasmacellcapableofproducingantibodyagainstaspecificantigenAntibodymarkstheantigenfordestructionbyotherimmunecells ANTIBODIES PlasmaglycoproteinsClassifiedbychemicalstructure biologicactivityIgG IgM IgA IgE orIgDProtecthostfromharmfulantigensRecognizeandbindwithantigensFunctions Opsonizebacteria neutralizetoxins virusesActivatesinflammatoryresponse ANTIBODYCLASSIFICATION IgG 80 plasmaIg inallbodyfluids secondaryresponse activatescomplementIgM Primaryresponse largemolecule vascularsystem activatescomplementIgA 95 ofbodysecretionIg respiratoryandGItract coatsbacteria somevirusesIgD Plasma Bcellsurfaces antigenreceptorIgE Hypersensitivityandallergicreactions asthma DevelopfromstemcellsthatmatureunderhormonalcontrolinthymusMakeupthecell mediatedimmuneresponseHelptodestroyinfectedcellsCoordinatetheoverallimmuneresponse TCELLS TYPESOFTCELLS CytotoxicTcellsKilltargetcellsdirectlyDelayedhypersensitivityTcellProduceslymphokinesthataffectothercells especiallymacrophages HelperTcellInducesBcellstoproduceantibodyRecognizeantigenfragmentsSuppressorTcellSuppressesantibodyproduction immunefunction T CELLRECEPTOR TcellhasmoleculeonitssurfacecalledT cellreceptorInteractswithmoleculescalledMHC majorhistocompatibilitycomplex Tcell lymphocyte withaT cellreceptoronitssurface ANTIBODYPRODUCTION FinalstageoftheprocessRequiresinteractionof BcellsHelperTcellsAntigen presentingcells HistocompatibilityAntigens HumanLeukocyteAntigens ProteinsfoundonthesurfaceofnearlyeverycellinthebodyRecognizessubstanceisforeign MajorHistocompatibilityComplex MHC MHC orHLAcomplex MajorgroupofgenesproducingtheHLAantigens4closelylinkedfocilocatedonshortarmofchromosome6 A B C Dcomplex AntigensproducedbyA B ClocifoundonsurfaceofmostcellsexcepterythrocytesDcomplexconsistsof3independentloci DR DP DQ ConfinedtoBcells macrophages someepithelialcells somestimulatedTlymphocytes INNATEIMMUNITY Nonspecific speciesspecific FirstlineofdefensePresentatbirthFoundinmulti cellularorganismsPermanentimmunityNotproductofimmuneresponse INNATEIMMUNITY EffectorsNeutrophilsMacrophagesEosinophilsNKcells MainMediatorsLysosomalenzymesCytokinesComplementproteinsAcutephaseproteins INNATEIMMUNITY ACQUIREDIMMUNITY Highlyspecific induciblediscriminatory unforgettingTlymphocyte dependentGainedafterbirth ActiveNaturalexposureImmunization ACQUIREDIMMUNITY PassiveDoesn tinvolvehost simmuneresponseAntibodies TcellstransferredtorecipientTemporaryimmunity ACQUIREDIMMUNITY Primary5 7daysafterexposureDominatedbyIgMLesseramountsofIgG Secondary2ndchallengebysameantigenRapidproductionofantibodyIgMsameproductionasprimaryIgGpredominant IMMUNERESPONSE HUMORALIMMUNITY AntigensstimulateBcells plasmacellsMediatedbyantibodiessecretedbyBcells CELL MEDIATEDIMMUNITY ActivationofsensitizedTcellsTcellssecretecytokinesTcellsbecomecytotoxiccellsTcellskillvirus infectedorabnormalhostcells ACUTEINFLAMMATORYRESPONSE Rapid nonspecificProtectiveresponsetocellularinjuryOccursonlyinvascularizedtissue MACROSCOPICHALLMARKSOFINFLAMMTION RednessHeatPainLossoffunctionoftheinflamedtissues Accumulationoffluidandcellsattheinflammatorysite MICROSCOPICHALLMARKSOFINFLAMMATION MASTCELLS MostimportantactivatorofinflammatoryresponseReleasesbiochemicalmediatorsHistamineChemotacticfactorsSynthesizesothermediatorsProstaglandinsLeukotrienesPlatelet ActivatingFactor PAF MAJORVASOACTIVEAMINESOFINFLAMMATION Histamine serotoninEffects ConstrictsvascularsmoothmusclesDilationofcapillariesRetractionofendothelialcellsliningcapillariesIncreasesvascularpermeability ACUTEPHASERESPONSE SystemicchangespresentifinflammationissevereenoughMaybetransient dissipatingwithrecoveryorpersistentinchronicdiseaseMediatedbyinflammation associatedcytokinesChangesinconcentrationsoflargenumberofplasmaproteins FeverSomnolenceAnorexiaChangesinplasmaproteinsynthesisAlteredsynthesisofendocrinehormones Hormoneseffected CRHGlucagonInsulinACTHCortisolCatecholaminesGrowthHormonesTSH ThyrpxineAldosteroneAVP ACUTEPHASERESPONSE Majoracutephaseproteins APP C Reactiveprotein CRP SerumamyloidA SAA NegativeAPPAlbuminTransthyretinTransferrin OtherpositiveAPPComplementproteinsFerritin 1 antitrypsin antiprotease FibrinogenFibronectinHempexinHaptoglobinCeruloplasmin ACUTEPHASEPROTEINS C REACTIVEPROTEIN Influencesinflammatory tissuerepairprocessesRecognizessomeforeignpathogensActivatescomplementsystemBondstophagocyticcellsInducesproductionofinflammatorycytokinesMaininitiatorofbloodcoagulationNeteffectmaybeantiinflammatory PLASMAPROTEINSYSTEM Inflammationismediatedby3keyplasmaproteinssystemsComplementsystemClottingsystemKininsystem COMPLEMENTSYSTEM The complementcascade Fig7 7 Activatedbyantigen antibodyreactions classicpathway Activatedbyotherproductsespeciallybacterialpolysaccharides alternate nonantibody pathway Producesbiologicallyactive anaphylacticorchemotactic fragmentsProducestargetcelllysisPhagocytosisIncreasesvascularpermeability CLOTTINGSYSTEM Extrinsic Intrinsicpathways Fig7 9 StopsbleedingLocalizesmicroorganismsProvidesameshworkforrepair healing KININSYSTEM BradykininmostimportantkininproteinDilatesvessels lowdosage Inducespain alongwithprostaglandins ContractsextravascularsmoothmuscleIncreasesvascularpermeabilityMayincreaseleukocytechemotaxis Fig7 6 INHIBITORYINFLAMMATORYENZYMES HistaminaseCarboxypeptidaseC1esytraseinhibitor 1 antitrypsin PhagocyticleukocytesNeutrophilsMacrophagesEosinophilsPlateletsLymphocytes CELLULARCOMPONENTSOFINFLAMMATION PHAGOCYTICCELLS Engulf destroymicroorganism Fig7 16 Encloseinphagocyticvacuoles phagolysosomes Toxicproducts degradativelysosomeenzymeskill digest OPSONINS Antibody complementcomponent C3b coatmicroorganisms Fig7 15 ThismakesthemmoresusceptibletophagocytosisBindsmicroorganismmoretightlytothephagocyte ENDOTHELIALCELLS Linethebloodvessels capillariesRetractduringinflammationPermitfluid nutrients phagocyticcellsintoareaofinjury POLYMORPHONUCLEARNEUTROPHIL PMN PredominantphagocyticcellinearlyinflammatoryresponseEntersinflammatorysitewithin6 12hoursAttractedbychemotacticfactorsShortlivedGraduallyreplacedbymacrophages lymphocytesPrimaryrole removalofdebris phagocytosis MONOCYTES LargestnormalbloodcellProducedinbonemarrowEnterscirculation migratestoinflammatorysiteDevelopsintoamacrophage MACROPHAGES Larger moreactivephagocyteCharacterizeschronicinflammationMayappearwithin24hoursofinjuryUsuallyarrive3 7dayslaterAttractedbychemotacticfactorreleasedbyPMN monocytesSurvivelongeratsite ROLEOFMACROPHAGES ResponsivetoproductssecretedbyTcellsParticipateinactivatingtheimmuneresponseStimulatesthegrowth differentiationofgranulocytes monocytesinbonemarrowProduceinflammatorycytokinesSecretesubstancestopromotewoundhealingPhagocyticactivity EOSINOPHILS ReleaseproductstocontrolinflammatoryresponseContainbiochemicalmediatorstocontroleffectsofhistamine serotoninContainsacausticproteinthatdissolvessurfacemembranesofparasitesInducedbyIgE mediatedmechanismsofhypersensitivity Fig7 18 CELLULARPRODUCTS InterleukinsLymphokinesChemokinesInterferonSeeFig7 19 INTERLEUKINS BiochemicalmessengersCytokinesproducedbymacrophagesorlymphocytesStimulatedbyantigensorinflammationStimulateotherleukocytestoproliferate immunefunction Chiefeffect theimmuneresponse LYMPHOKINES CytokinesproducedbyTcellsAlsobiochemicalmediatorsMostimportanteffectsonmacrophagesTumornecrosisfactor TNF CHEMOKINES GenerallyproinflammatorycytokinesEffectsonleukocytesChemotaxisGrowthActivationReleasestoredchemicalsfromintracellularstoragegranules degranulation INTERFERON DefenseagainstviralinfectionsCytokineproduced releasedbyhostcellsinvadedbyvirusPreventsvirusfrominfectinghealthycellStimulatesuninfectedcellstoproduceantiviralproteins Fig7 20 INF INF areantiinflammatoryINF isproinflammatoryandenhancescell mediatedimmunity CHRONICINFLA