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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 1样细胞受抑制
Objective: To investigate the mechanisms of nasal tolerance and Wistar rats tolerance to experimental autoimmune myasthenia gravis (EAMG). Methods: [3H] TdR incorporation and ELISpot assay. RESULTS: The AChR-specific lymphocyte proliferation (LPR) stimulated index in the porcine and inguinal lymph nodes (PILN) of EAMG rats at 3, 5 and 7 weeks after immunization was higher than that in nasal rats, 7 weeks higher than Wistar rats (P <0 05). At 5 and 7 weeks after immunization, the number of AChR-reactive interferon-γ secreting cells in PILN of EAMG rats was higher than that of nasal tolerant rats and Wistar rats (P <0.05). CONCLUSION: Immune response of lymphocytes to AChR is enhanced when EAMG occurs, and Th1-like cells that secrete IFN-γ are increased. Immune response of lymphocytes to AChR was decreased at EAMG tolerance, and Th1-like cells secreting IFN-γ were inhibited