B细胞在MOG_(35-55)诱导的小鼠实验性自身免疫性脑脊髓炎中的作用  

Role of B cells in experimental autoimmune encephalomyelitis in mice induced by myelin oligodendrocyte glycoprotein_(35-55)

作　　者：詹晓霞[1] 杨金凤[1] 刘宇[1] 王心悦[1] 谢晓丽[1] 孙博[1] 李呼伦[1] 

机构地区：[1]哈尔滨医科大学神经生物学教研室黑龙江省高校神经生物学重点实验室,黑龙江哈尔滨150081

出　　处：《中国生物制品学杂志》2013年第3期340-345,共6页Chinese Journal of Biologicals

基　　金：国家自然科学基金(81171121);黑龙江省自然科学基金(LC2011C14);黑龙江省研究生创新科研项目(YJSCX 2011-347HLJ)

摘　　要：目的探讨B细胞参与MOG35-55诱导的实验性自身免疫性脑脊髓炎(Experimental autoimmune encelphalomyelitis,EAE)小鼠模型的可能机制。方法采用MOG35-55肽段免疫C57BL/6小鼠建立EAE模型;采用临床评分检测EAE模型建立情况,HE和快蓝染色观察脊髓炎性细胞浸润和脱髓鞘状况,流式细胞术检测B细胞活化程度,免疫组化法检测脾组织生发中心的形成,ELISA法检测IgG1、IgG2a和IgG2b的分泌水平。结果成功建立了MOG35-55诱导的EAE小鼠模型,EAE组临床评分明显高于弗氏完全佐剂(Complete Freund adjuvant,CFA)组(P<0.001),EAE组小鼠脊髓可见明显的炎性细胞浸润和脱髓鞘斑块;在EAE组发病起始期(免疫后第5天和第8天),外周免疫器官活化B细胞表达水平明显高于CFA组(P<0.01);在发病高峰期(免疫后第15天)EAE组小鼠脾中形成生发中心,而CFA组未见生发中心形成,且外周血抗MOG35-55抗体分泌水平明显高于CFA组(P<0.005)。结论 MOG35-33肽段可以诱导B细胞活化,进而可能通过发挥体液免疫作用介导EAE疾病的发生。Objective To investigate the possible mechanism of B cells in mediation of myelin oligodendrocyte glycoprotein35-55（MOG35-55） induced experimental autoimmune encephalomyelitis（EAE） in mice. Methods Mouse model was established by immunizing C57BL/6 mcie with MOG35-55 and evaluated by clinical scoring. The inflammatory cell infiltration and demyelinatioan were observed by HE and fast blue staining, while the activation of B ceils by flow cytometry, the formation of germinal centres by immunohistochemical assay, and secretion levels of IgG1, IgG2a and IgG2b by ELISA. Results Mouse model of EAE was successfully established, of which the clinical scores were significantly higher than those of control mice immunized with complete Freunds adjuvant （CFA）（P 〈 0. 001 ）. Obvious inflammatory cell infiltration and demyelination of spinal cord were observed in the model mice. The expression levels of activated B cells in secondary lymphoid organs of mice in EAE group at the initial phase of the disease （on days 5 and 8 after immunization） were significantly higher than those in CFA group （P 〈 0. 01）. However, germinal centers were found in mice in EAE group at peak period of disease （on day 15 after immunization） while were not in those in CFA group, and the secretion level of antibody against MOG35-55 in peripheral blood of the former were significantly higher than that in C FA group （P 〈 0. 005）. Conclusion MOG3,55 peptide may induce the activation of B cells thus mediate the onset of EAE by hormoral immunity.

关 键 词：B淋巴细胞 实验性自身免疫性脑脊髓炎 多发性硬化 

分 类 号：R593.2[医药卫生—内科学] R744.3[医药卫生—临床医学]