NK1.1+细胞在实验性重症肌无力发病机制中的作用.pdf

·38· ·神经内分泌与免疫· NKl．1+细胞在实验性重症肌无力发病机制中的作用① 王菁华孙博李国忠⑦王丹丹刘玉梅王琪穆莉莉金连弘李呼伦 (哈尔滨医科大学神经生物教研室哈尔滨医科大学神经生物学黑龙江省高校重点实验室，哈尔滨150081) 中国图书分类号11392．3文献标识码A 文章编号1000-484X(2008)01-0038-05 [摘要]目的：探讨NKI．1+细胞在重症肌无力疾病进展中发挥的作用以及其调节机制。方法：(1)用腹腔注射抗 和对照组小鼠之间实验性自身免疫性重症肌无力(EAMG)的发病情况和病情严重程度的区别；(3)观察淋巴细胞增殖以及应 用ELISA方法检测细胞因子TGF—B、抗AchR IgG、 AchR 特异性T细胞产生TGF—B的增加，从而抑制了重症肌无力的进展。 [关键词]实验性自身免疫性重症肌无力；NKl．1+细胞；细胞因子；TGF-B EffectofNKl．1+cellsontheoutcomeofthe of auto． developmentexperimental immune myastheniagravis WANG Jing—Hua，sUNBo，LIGuo—Zhong，WANGDan—Dan，LIUYu-Mei，WANGQi，MULi—Li，JINLian-Hong， LI 15008 1，China Hu．Lun．DepartmentofNeurobiology。Harb讯MedicalUniversity。Harbin the effectofNKl．1+ceUsinthe of autoim- [Abstract]Objective：Toinvestigateimmunoregulation developmentexperimental mune invivo ofNKl．1+cellsand toNKl．1and myastheniagrads(EAMG)．Methods：(1)For TGF-B，antibodiesTGF—B depletion wereadministered toeach determinetheincidenceand ofEAMGinNKI．1+ byintraperitoneal(i．P．)injecfionmouse；(2)To sevedty disease were cell wasobservedandthe of of cell-depletedmice，the symptomsgraded；(3)Tproliferation cytokinesTGF一8，isotypes anti-AChRweremedlsured ELISA onsetofEAMGWag andthe Wagdecreasedobvi— IgG byusing kit．Results：(1)The delayed severity micewithcontrolmice．OtherwiseofNKl．1+cellsfrom 7afterimmunizationhad ouslycomparingNKI．1+cell—depleted depletion day no onthe of ofNKI．1+ceilsdidnot alterTcell toAChR．