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为探讨T细胞对乙酰胆碱受体(AChR)免疫应签在实验性自身免疫性重症肌无力(EAMG)发病中的作用,本文用酶联免疫斑点技术(ELISPOTS)和[3H]TdR掺入法检测Lewis大鼠和Wistar Furth(Wistar)大鼠AChR加完全弗氏佐剂(CFA)免疫后不同时间点 窝和腹股沟淋巴结(PILN)、脾脏及胸腺中AChR反应性r干扰素分泌细胞和淋巴细胞增生反应。结果表明:免疫后第5周PILN中AChR反应性r干扰素分泌细胞Lewis大鼠为8.9±1.5,Wistar大鼠为4.3±0.9;第7周Lewis大鼠为7.8±1.2,Wistar大鼠为4.2±1.6,差异均有显著性(P<0.05);免疫后第7周PTLN中淋巴细胞增生反应(SI)Lewis大鼠为6.83±2.14,Wistar大鼠为2.62±1.07,差异具有显著性(P<0.05)。与此相一致,lewis大鼠免疫后出现典型的EAMG,而wistar大鼠不出现EAMG。结果提示,T细胞对AChR的应答在EAMG的发病过程中起重要作用。PILN中T细胞对AChR免疫应答的抑制,可阻止EAMG的发生。
In order to investigate the role of T cells in the induction of AChR in experimental autoimmune myasthenia gravis (EAMG), ELISPOTS and [3H] TdR incorporation Lewis rats and Wistar rats (Wistar) rats AChR plus complete Freund’s adjuvant (CFA) immunized at different time points and inguinal lymph nodes (PILN), spleen and thymus AChR reactivity r interferon-producing cells and lymphocyte proliferation reaction. The results showed that the percentage of AChR-reactive interferon-secreting cells in PILN was 8.9 ± 1.5 in Wistar rats and 4.3 ± 0.9 in Wistar rats at week 5 after immunization, 7.8 ± 1.2 in Lewis rats at week 7 and 4.2 at Wistar rats ± 1.6, respectively (P <0.05). In the 7th week after immunization, the lymphocyte hyperplasia (SI) in PTLN was 6.83 ± 2.14 in Lewis rats and 2.62 ± 1.07 in Wistar rats, the difference was significant (P <0.05) <0.05). Consistent with this, typical EAMG is present in lewis rats after immunization, whereas no EAMG appears in wistar rats. The results suggest that the response of T cells to AChR plays an important role in the pathogenesis of EAMG. The inhibition of AChR immune responses by T cells in PILN can prevent the occurrence of EAMG.