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目的探讨IFN-γ和IL-33在实验性自身免疫性神经炎(EAN)发病机制中的作用及EAN中的Th1/Th2细胞极化。方法用P253-78肽段免疫Lewis大鼠,建立EAN模型,观察其发病情况和组织病理改变,并检测淋巴细胞增值反应,用RT-PCR技术检测干扰素γ(IFN-γ)和白介素33(IL-33)在大鼠发病高峰期脾脏、淋巴结和坐骨神经中的表达。结果EAN组大鼠临床表现明显,病理检查可见大量炎性细胞浸润;坐骨神经组织、淋巴结,脾脏中IFN-γmRNA表达显著升高,IL-33mRNA表达明显减少,其引流淋巴结淋巴细胞对P253-78aa的刺激发生强烈的淋巴细胞增殖反应。结论IFN-γ对EAN发病起促进作用,IL-33对EAN大鼠起保护作用;EAN中Th0细胞向Th1的转化明显增强而向Th2细胞的转化则受到抵制。
Objective To investigate the role of IFN-γ and IL-33 in the pathogenesis of experimental autoimmune neuritis (EAN) and the Th1 / Th2 cell polarization in EAN. Methods Lewis rats were immunized with P253-78 peptide to establish EAN model. The incidence and histopathological changes were observed. Lymphocyte proliferation reaction was detected. The levels of IFN-γ and IL-33 IL-33) in the spleen, lymph node and sciatic nerve at the peak of the onset of the rat. Results The clinical manifestations of rats in EAN group were obvious, and a large number of inflammatory cells infiltrated in the pathological examination. The expression of IFN-γmRNA in sciatic nerve tissue, lymph nodes and spleen was significantly increased, and the expression of IL-33 mRNA was significantly decreased. The numbers of draining lymph node lymphocytes in P253-78aa Stimulation of intense lymphocyte proliferation reaction. Conclusions IFN-γ can promote the development of EAN, and IL-33 can protect EAN rats. In EAN, the transformation of Th0 cells to Th1 and Th2 cells are resisted.