Th17及IL-17与实验性自身免疫性重症肌无力发病过程的相关性

Pathogenetic Role of Th17 and IL-17 in Experimental Autoimmune Myasthenia Gravis

目的探讨Th17及其相关因子IL-17与实验性自身免疫性重症肌无力(EAMG)发病过程的相关性。方法建立EAMG大鼠模型及CFA对照组,分别于两发病时相(早期发病高峰和晚期发病高峰),采用ELISA法检测血清以及淋巴细胞培养上清中IL-17的含量;流式细胞仪检测CD4+IL-17+淋巴细胞含量;3H增殖试验检测淋巴细胞的增殖能力;B-ELISPOT法检测B细胞的抗体分泌情况。结果与CFA组相比,EAMG组大鼠血清、淋巴细胞培养上清中IL-17的表达以及CD4+IL-17+淋巴细胞含量在早期发病时相差异均无统计学意义;而在晚期发病时相则均明显增多。与非刺激组相比,IL-17的刺激对CFA和EAMG组淋巴细胞的增殖能力及B细胞抗体分泌水平,在早期发病时相均无明显影响;而在晚期发病时相,EAMG组均明显升高。结论Th17及其相关因子IL-17参与大鼠EAMG的晚期发病时相,并促进疾病的发展。

Objective To investigate the participation of Thl7 and its correlation cytokine IL-17 in the occurrence and development of experimental autoimmune myasthenia gravis （EAMG）. Methods The rat model of EAMG was established by injecting R- AChR at tail root, using CFA as control. The rats in test and control groups were determined at two phases, i.e. early and late peaks of onset, for IL-17 contents in sera and culture supernatant of lymphocytes by ELISA, for CD4＋IL-17＋ lymphocytes content by flow cytometry, for proliferation level of lymphocytes by 3H-thymidine incorporation, and for antibody level secreted by B cells by B-ELISPOT method. Results The expression levels of IL-17 in sera and culture supernatant of lymphocytes of rats and CD41L-17 lymphocyte content in EAMG group showed no significant difference with those in control group at early peak of onset, while increased significantly at late peak. The lymphocyte proliferation level and antibody level secreted by B cells stimulated by IL-17 in EAMG and control groups showed no significant difference with those by PBS at early peak of onset, however, at the late peak, both the levels in EAMG group increased significantly. Conclusion Th17 and IL-17 mainly participate the late onset of EAMG and promote the progress of the disease.