诱导EAMG耐受性机制初探  

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

作　　者：梁丽云[1] 丰玲[1] 马存根[1] 

机构地区：[1]大同医学专科学校,037008

出　　处：《大同医学专科学校学报》2000年第1期1-5,共5页Journal of Datong Medical College

基　　金：山西省归国留学基金

摘　　要：目的：探讨鼻腔耐受和Ｗｉａｔａｒ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Ｇｕｏ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．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.

关 键 词：理症肌无力 免疫耐受 Th1样细胞 

分 类 号：R746.103[医药卫生—神经病学与精神病学]