再生障碍性贫血免疫发病机制的探讨

Studyonthepathogenesisofaplasticanemia

采用免疫磁珠结合ＣＦＵ－ＧＭ及骨髓基质细胞集落培养法对１０例慢性再生障碍性贫血（慢性再障）患者的免疫发病机制进行探讨。结果正常对照组ＣＦＵ－ＧＭ集落生长高峰为培养第７天，其集落数为１７０．４±８６．４／２×１０５，基质细胞集落生长高峰为第１４天，集落数为７９．０±４０．０／８×１０６。正常骨髓单个核细胞（ＭＮＣ）加患者血清组ＣＦＵ－ＧＭ的第７天集落数为４５．９±３４．４／２×１０５，基质细胞第１４天集落数为３０．１±１９．４／８×１０６，与正常对照组比较，均有明显差异（Ｐ＜０．０１）。１０例再障中，６例ＣＦＵ－ＧＭ生长欠佳，８例基质细胞生长欠佳。剔除ＩｇＧ前、后的患者血清组比较，其ＣＦＵ－ＧＭ及基质细胞生长情况无显著性差异。剔除患者骨髓ＭＮＣ内的ＣＤ４细胞组：１０例的ＣＦＵ－ＧＭ均生长欠佳，８例的基质细胞生长欠佳。剔除患者骨髓ＭＮＣ内的ＣＤ８细胞组：１０例中只有２例的ＣＦＵ－ＧＭ及基质细胞生长欠佳，其余均生长良好。提示患者血清影响正常ＣＦＵ－ＧＭ及基质细胞的生长，这种影响与ＩｇＧ关系不大；ＣＤ４细胞的减少或异常与再障发病有关，ＣＤ４有促进造血作用，ＣＤ８细胞有抑制造血作用；基质细胞异常在再障发病中有重要作用?

BonemarrowCFU-GMandstromalcel(SC)colonyculturewereusedtostudythepathogenesisin10chronicaplasticanemia(AA)patients.Inthecontrolgroup,thepeakvaluesofCFU-GMcolonieswereatthe7thdaywithameanof170.4±86.4/2×105cels,andthepeakvaluesofSCcolonieswereat14thdaywithameanof79.0±40.0/8×106cels.WhenserafromAApatientswereaddedtothecultureofnormalCFU-GMandSC,thepeakvalueswerereducedto45.9±34.4/2×105celand30.1±19.4/8×106cels,respectively(P<0.01).RemovalofIgGfromtheseragavethesameCFU-GMandSCcolonyyieldsasthosewithintactser-a.Outofthe10bonemarrowsamplesfromAApatients,thegrowthofCFU-GMin6andSCin8werepoor.WhenCD4+celsweredepletedfromthemononuclearcelsofthepatients′bonemarrow,thegrowthofCFU-GMin10casesandofSCin8casesremainedpoor,whileremovalofCD8+celsgavenor-malcolonyyieldsofCFU-GMinal10andSCin8/10patients.Inconclusion,AApatient′sserainhibitedthegrowthofnormalCFU-GMandSC,andtheinhibitionhadlittlerelationshiptoserumIgG.TheabnormalitiesofCD4+andCD8+celswereassociatedwiththegenesisofAA.