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作 者:梁丽云[1,2,3] 马存根[1,2,3] 张光先 肖保国[1,2,3]
机构地区:[1]大同医学专科学校 [2]河南医科大学附属一院神经科 [3]上海医科大学华山医院
出 处:《中国免疫学杂志》1998年第3期187-189,共3页Chinese Journal of Immunology
摘 要:用AChR加CFA免疫大鼠后,Lewis大鼠出现典型的临床肌无力,而WistarFurth(W.F)大鼠不出现任何症状。为阐明W.F大鼠对AChR耐受的机制,检测了表达IFN-γ、IL-4和TGF-βmRNA的MNC和肌肉AChR。结果表明,W.F大鼠免疫后第5、7周PILN中AChR诱导的IFN-γmRNA表达细胞数比Lewis大鼠低,TGF-βmRNA表达细胞数比Lewis大鼠高,肌肉AChR含量比Lewis大鼠高。提示IFN-γ和TGF-β与EAMG的发生有关,TGF-β上调可抑制IFN-γmRNA表达,减少肌肉AChR丢失。fter immunization with AChR plus CFA, Lewis rats displayed the typical signs of EAMG, while Wistar Furth(WF) rats did not present any signs of EAMG. To clarify the mechanism of WF rats tolerance to AChR and the effect of cytokines in tolerance, in situ hybridization with radiolabelled cDNA oligonucleotide probes was adopted to enumerate mononuclear cells(MNC) expressing mRNA for interferonγ(IFNγ), interleukin4(IL4) and transforming growth factorβ, radioimmunoassay was used to examine the muscle AChR content. The results showed that WF rats had lower numbers of AChRinduced IFNγ mRNA expressing cells and higher numbers of AChRinduced TGFβ mRNA expressing cells in MNC isolated from popliteal and inguinal lymph nodes(PILN) compared to Lewis rats after immunization at the fifth week and the seventh week. Muscle AChR content was higher in WF rats than that in Lewis rats. The results suggested that IFNγ and TGFβ were involved in the development of EAMG; TGFβ upregulation could inhibit IFNγ mRNA expression and decrease muscle AChR loss, further prevent and suppress the occurrence of EAMG.
分 类 号:R746.1[医药卫生—神经病学与精神病学]
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