IgG抗体ppt课件.ppt

IgG抗体ANTIBODY,1,免疫球蛋白的结构,（StructureofAbMolecules）,2,同种异型（allotype)：同一种属不同个体间免疫球蛋白分子所具有的不同的抗原特异性标志。,由C区决定，主要反映在Ig分子的CH和CL上的一个或数个氨基酸的差异，又称为遗传标志。,3,独特型(idiotype,Id)：同一个体内不同B细胞克隆产生的免疫球蛋白分子所特有的抗原特异性标志。,由超变区决定,4,IgG分子的四种亚型,IgG1,IgG4,IgG3,IgG2,5,主要以单体形式存在，抗原结合价为2价出生后3个月开始合成，35岁接近成人血清中含量最高，占血清总Ig的75-80%产生比较晚，是再次应答的主要抗体半衰期最长(t23天)分布最广，易通过毛细血管壁，是血管外的主要抗体唯一能通过胎盘的Ig，新生儿抗感染免疫起重要作用激活补体IgG13（经典），IgG4（替代）结合细胞吞噬细胞调理作用NK细胞，吞噬细胞介导ADCC结合SPA协同凝集实验,特性：又称为胎盘球蛋白,6,功能：,抗感染的主要抗体,新生儿抗感染免疫的重要抗体介导II,III型超敏反应介导自身免疫,7,功能,IgG抗体是反映人体免疫功能的重要指标。根据结构的不同IgG抗体可分为4个亚类,即IgG1,IgG2,IgG3和IgG4。这4个亚类的生物学特性不同,因此它们在疾病的发生发展过程中发挥不同的作用.,8,功能,针对细菌和病毒抗原产生的抗体中(例如破伤风毒素或膜蛋白成分都是T细胞依赖型抗原),IgG1占主导地位,有时伴随IgG3的产生,IgG2水平较低。,9,功能,特异性皮炎(atopicdermatitis)是一种慢性复发性皮肤炎症疾病,特异性皮炎患者血清中针对花粉或尘螨的特异性IgE和IgG4水平升高。,10,功能,青霉素过敏患者血清中,IgG3和IgG4阳性的百分率分别为28.05%,13.39%和12.80%,表明IgG3和IgG4抗体在青霉素超敏反应中发挥重要作用。,11,IgG抗体与HDN,各亚类激活补体经典途径的能力为IgG3IgG1IgG2,所以IgG3在各亚类中溶血性最强,发生的HDN最严重。,12,IgG抗体与HDN,从患儿及患儿母亲血清中IgG亚类含量的构成来看,虽均以IgG1为主,但患儿体内IgG1的比例较母亲体内高,而其他3种亚类均略低于母体,说明了IgG1含量升高对新生儿溶血病有着更重要的作用。,13,IgG抗体与HDN,孕妇血清中IgG特异性抗体效价持续升高,并且IgG1亚类含量也显著高者,可预报新生儿溶血病的发生,当IgG3也显著升高时,提示新生儿溶血严重。,14,Theimmunesystemconsistsoftwofunctionalcomponents:InnateimmunesystemPreventspenetrationandspreadofinfectiousagentsbyavarietyofphysical,biochemicalandcellularbarriers(skin,mucosa,lysozymes,complement,phagocytes)AdaptiveimmunesystemDevelopsaspecificimmunologicalmemoryafterthefirstattack.Thisleadstoastronger,fasterandmoreeffectiveresponseuponrenewedcontactwiththesameagent.LymphocytesandimmununoglobulinsarethekeyelementsHumoralimmunityB-cellsplasmacellsimmunoglobulinsCellmediatedimmunityT-cellsHelperT-cells&CytotxicT-cells,15,InhumoralimmunityB-cellsrecognizesolubleorcellsurfaceantigens(onextracellularmicrobes)anddifferentiateintoantibodysecretingplasmacells.Incell-mediatedimmunityhelperT-cellsrecognizeantigensonthesurfacesofantigen-presentingcellsandsecretecytokines,whichstimulateB-cellsandT-cells.CytotoxicT-cellsrecognizeantigensoninfectedcellsandkillthesecells.,16,17,18,19,20,relativeserumconcentrationsIgG1IgG2IgG3IgG4differencesinflexibilityoftheIgG3IgG1IgG4IgG2hingeregiondifferencesinbiologicalpropertiesFabpart+antigeneffectorfunctionsviaFcpartactivationofcomplementIgG3IgG1IgG2IgG4inductionofphagocytosisFcgRICD64:IgG3IgG1IgG4(opsonisation)FcgRIICD32:IgG3IgG1IgG2bindingtoFcgRofeffectorcellsFcgRIIICD16:IgG3=IgG1CD16:neutrophilgranulocytes,monocytes,macrophages,NKcellsCD32:monocytes,subpopulationofmacrophages,granulocytes,eosinophils,BcellsCD64:monocytes,activatedgranulocytes,21,IgG1MainresponsetovirallandbactteriallprotteinanttigenexposureImmuneresponsettocapsullepollysaccharideActtivattiioncompllementtEfffiicienttbindingttollymphocyttesviaFcrecepttorAuto-antibodiesIgG2PredominantimmuneresponsettopollysacchariideantigensofbactteriasuchaspneumococcigroupAsttreptococciandHaemophillusiinfflluenzeaIgG3High-affiniittyantbodiesttoproteinantigensstrongestcompllementtacttiivattiionefficienttbindiingtolymphocytesviiaFcrecepttorauto-antibodiiesIgG4ResponsestochronicallergicstimullationImmuneresponsettoalergensevenafterhyposensitizationBlockingtheIgEresponse,22,decreaseofoneIgGsubclass+increaseofothersubclasstotalIgGlevelmaynormal.determinationofIgGsubclasslevelsisimportant,evenwhenthetotalIgGleveliswithinoronlyslightlybelowthereferencerangeofhealthyindividuals.IgGsubclassdeficiencyisnotexcludedbyanormalorevenhightotalIgGconcentration!ThefindingofadecreasedlevelofoneoftheIgGsubclassescanneverprovideadefinitediagnosis,butshouldratherbeconsideredasanindicationofadisturbanceoftheimmunesystem,requiringfurtherdiagnosticinvestigation.,23,Autoimmune/atopicdiseasesBronchialasthmaIgG2,IgG3DiabetesvariableIdiopathicthrombocytopenicpurpuraIITPIgG2,IgG4SystemiclupuserythematosusIgG3,IgG4ImmunodeficienciesBonemarrowtransplantationIgG2,IgG4CVID(commonvariableimmunodeficiency)IgG1,IgG2,IgG4High-dosecorticosteroidsIgG2,IgG3HIVinfectionIgG2,IgG4Chemotherapy,radiationexposureIgG2Wiskott-AldrichdiseaseIgG4InfectionsOtitismedia(pneu