【摘要】 目的:探讨鼻腔耐受和Wistar大鼠对EAMG耐受的机理。方法:[~3H]TdR掺入和酶联免疫斑点法。结果:免疫后第3、5、7周EAMG大鼠腘窝和腹股沟淋巴结(PILN)中AChR特异的淋巴细包增生反应(LPR)刺激指数比鼻腔耐受大鼠高,第7周比Wistar大鼠高(P<0.05)。免疫后第5、7周EAMG大鼠PILN中AChR反应性γ干扰素分泌细胞数比鼻腔耐受大鼠和Wistar大鼠高(P<0.05)。提示:EAMG发生时淋巴细胞对AChR的免疫应答增强,分泌IFN—γ的Th1样细胞增多。EAMG耐受时,淋巴细胞对AChR的免疫应答降低,分泌IFN—γ的Th1样细胞受抑制。更多还原

【Abstract】 AIM: To explore the mechanism of immune tolerance to experimental autoimmune myasthenia gravis (EAMG) in nasally tolerized rats and Wistar rats. METHOD: [3 H]thymidine incorporation and solid-phase ELISPOT assay were used. RESULT: The stimulative index of lymphocyte proliferation responses to AChR in popliteal and inguinal lymph nodes (PILN) of EAMG rats was higher than that of nasally tolerized rats on week 3, 5 and 7post immunization (p. i. )with AChR plus complete Freund’s adjuvant (CFA), and was higher than that of Wister rats on week 7 p. i. (P<0. 05). The values of AChR reactive IFN-r -secre ting cells in PILN of EAMG rats was higher than that of nasally tolerized rats and Wistar rats on week 5 and 7 p. i. (p<0. 05). CONCLUSION: When EAMG occured the lymphocyte immune response to AChR enhanced and Th1 like cells of secreting IFN-r increased. When tolerance to EAMG happened the lymphocyte immune response to AChR reduced and Thl like cells of secreting IFN-r were suppressed.更多还原