诱导实验性自身免疫性重症肌无力耐受性的机制初步探讨

A preliminary study of the mechanisms of immune tolerance to experimental autoimmune myasthenia gravis

目的 :探讨鼻腔耐受和Wistar大鼠对实验性自身免疫性重症肌无力 (EAMG)耐受的机制。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 月国 窝和腹股沟淋巴结 (PILN)中乙酰胆碱受体 (AChR)特异的淋巴细胞增生反应 (LPR)刺激指数比鼻腔耐受大鼠高 ,第 7周比Wistar大鼠高 (P <0 0 5 )。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 .0 5 )。结论 :EAMG发生时淋巴细胞对AChR的免疫应答增强 ,分泌IFN -γ的Th 1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Th

AIM: To explore the mechanism of immune tolerance to experimental autoimmune myasthenia gravis (EAMG) in nasally tolerized rats and Wistar rats. METHOD: [ 3H] thymidine incorporation and solid-phase ELISPOT assay were used. RESULTS: The stimulative index of lymphocyte proliferation responses to acetylcholine receptor (AChR) in popliteal and inguinal lymph nodes (PILN) of EAMG rats was higher than that of nasally tolerized rats on week 3, 5 and 7 post immunization (PI) with AChR plus complete Freund′s adjuvant (CFA), and was higher than that of Wistar rats on week 7 PI ( P <0.05). The values of AChR-reactive interferon(IFN)-γ-secreting cells in PILN of EAMG rats was higher than that of nasally tolerized rats and Wistar rats on week 5 and 7 PI ( P <0.05). CONCLUSIONS: When EAMG occured the lymphocyte immune response to AChR enhanced and secreting IFN γ by Th l like cells increased. When tolerance to EAMG happened the lymphocyte immune response to AChR reduced and Thl like cells of secreting IFN γ were suppressed.