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机构地区:[1]大同医专生化教研室,037008 [2]大同医专
出 处:《大同医专学报》1999年第2期4-7,共4页
基 金:山西省归国留学人员基金
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Wister,Furth(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,本文检测了表达IFN—γ,IL—4和TGF—β mRNA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—γ mRNA表达细胞数比Lewis大鼠低,TGF—β mRNA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,进而预防和抑制EAMG发生。After immunization with ACHR Plus CFA, Lewis rats displayed the typical signs of EAMG,while Wistar Furth(WF) rats did nor present any signs of EAMG. To clari fy the meehanism of WF rats tolerance to ACHR and the effect of cytokines in tolerance, in situ hybridization with radiolabcllcd cDNA oligonuclcotidc probes was adopted to enumerate mononuclear cells (MNC,) expressing mRNA for interferon-γ (IFN-γ) ,interlenkin-4 (IL-4) and transforming growth factor-β,radioimmunoassay was used to examine the muscle ACHR content. The results showed that WF rats had lower numbers of ACHR-induced IFN-γ mRNA expressing cells and higher numbers of AChR - induced TGF - β , mRNA expressing cells in MNC isolated from popliteal and inguinal lymph nodes(PILN) compared to Lewis rats af ter immunization at the fifth week and the seventh week,Muscle AChR content was higher in WF rats than that in Lewis rats. The results suggest that IFN-γ and TGF-β are involved in the development of EAMG;TGF-β uregulation can inhibit IFN-γ mRNA expression and de-crease muscle AChR loss,further prevent and suppress the occurrence of EAMG.
关 键 词:重症肌无力 乙酰胆碱受体 TGF-Β 大鼠 CFA
分 类 号:R746.1[医药卫生—神经病学与精神病学]
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