iga nephropathy iga nephropathy umf 肾小球疾病的免疫球蛋白iga肾病免疫球蛋白iga肾病 课件

iga nephropathy iga nephropathy umf 肾小球疾病的免疫球蛋白iga肾病免疫球蛋白iga肾病 课件

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大小:3.54 MB

页数:109页

时间:2018-10-07

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1、Glomerulopathies–IgAnephropathyIgAnephropathy-PathogenesisGlomerulopathies–IgAnephropathyIgAnephropathy-PathogenesisMesangialIgApromotesglomerularinflammationaseriesofevents…….cancauseendstagerenaldiseaseGlomerulopathies–IgAnephropathyGlomerulopathies–IgAnephropathyIgAnephropa

2、thy-PathogenesisWhatspecificmechanismsinfluencethedepositionofIgAanditsinitiationofinflammation?Glomerulopathies–IgAnephropathyGlomerulopathies–IgAnephropathyIgAnephropathy-PathogenesistightlyTcellcontrolledprocessesinhealthmostpolymericIgAisproducedinthemucosalimmunesystemisinvol

3、vedinmucosaldefensethebonemarrowproducesmonomericIgA,whichreachesthecirculationGlomerulopathies–IgAnephropathyGlomerulopathies–IgAnephropathyIgAnephropathy-PathogenesisinIgAnephropathysynthesisofpolymericIgAisincreasedinthebonemarrowanddecreasedinthemucosaGlomerulopathies–IgAnephr

4、opathyGlomerulopathies–IgAnephropathyGlomerulopathies–IgAnephropathyIgAnephropathy-PathogenesisYesitisGlomerulopathies–IgAnephropathyIgAnephropathy-PathogenesisWhymightthishappen?ThisprocessisverytightlyTcellregulatedInresponsetoamucosalantigen,Tcellsreachthecirculation,butwillret

5、urntothemucosatosynthesizepolymericIgAiftheyexpressalpha4beta7,themucosalhomingreceptorIfontheotherhand,asystemicantigenisconfronted,Tcellswillhometothemarrowiftheyexpressthealpha4beta1systemichomingreceptorGlomerulopathies–IgAnephropathyGlomerulopathies–IgAnephropathyGlomerulopat

6、hies–IgAnephropathyIgAnephropathy-PathogenesisinIgAnephropathy-theseprocessesisabnormalthereisanexaggerationofsystemichomingreceptorexpression,whichwoulddriveTcellsnotbacktothemucosabuttowardsthemarrowtheabnormalsiteofIgA1production,whichisoneofthefeaturesofIgAnephropathyGlomerul

7、opathies–IgAnephropathyGlomerulopathies–IgAnephropathyIgAnephropathy-PathogenesisinIgAnephropathy-theseprocessesisabnormalbutnotonlythereisanexaggerationofsystemichomingreceptorexpression,whichwoulddriveTcellsnotbacktothemucosabuttowardsthemarrowtheabnormalsiteofIgA1production,wh

8、ichisoneofthefeaturesofIgAnephrop

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