文档介绍：MRL/lpr狼疮小鼠CD4+CD25+调节性T细胞和相关基因的研究
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作者:卢雪红田庚杨巍李一顾华
【摘要】目的通过研究MRL/lpr系统性红斑狼疮(SLE)小鼠(模型组)胸腺、脾脏中CD4+CD25+调节性T细胞(Tr)数量和相关基因的变化,探讨Tr在SLE发病中的作用。方法采用间接免疫荧光法检测模型组和对照组血清中抗核抗体水平,流式细胞术检测胸腺、脾脏中Tr数量,RTPCR检测Tr功能基因表达水平。结果抗核抗体模型组均为阳性,而对照组均为阴性;胸腺、脾脏中Tr数量模型组与对照组无明显差别;Foxp3的表达水平在模型组胸腺中与对照组无明显差别,而在模型组脾脏中却低于对照组;CTLA4的表达水平在模型组胸腺和脾脏均高于对照组。结论 Tr数量的变化在MRL/lpr小鼠的发病中不起关键作用,而Tr功能的变化,尤其在外周的功能缺陷可能是其发病的原因之一,至于Tr的抑制功能是否真正发生变化,还有待于进一步通过体外抑制功能的检测来确定。
【关键词】 MRL/lpr小鼠;系统性红斑狼疮;CD4+CD25+调节性T细胞;小鼠
【Abstract】Objective To investigate CD4+CD25+ regulatory T cells and target genes in thymus and spleen of MRL/lpr mice. Methods Serum anti
nuclear antibody was detected by indirect immunofluorescence. CD4+CD25+Tr was determined by flow cytometry and its target genes were detected by RTPCR. Results Antinuclear antibody was positive in model group but negative in control group. There were no significant differences of CD4+CD25+Tr in model and control groups. Foxp3 levels of model group was no significant difference in thymus but lower in pared with that of control group. CTLA4 levels of model group had higher than those of control group both in thymus and in spleen. Conclusions MRL/lpr mice do not occur as a result of reduced level of CD4+CD25+Tr, but function defect of CD4+CD25+Tr may be responsible for its occurrence. But the suppressive effect of CD4+CD25+Tr is st