CD52单克隆抗体通过抑制Th1/17介导的炎症及诱导调节性T细胞反应对克罗恩病模型小鼠结肠炎的治疗作用
Anti-mouse CD52antibody ameliorates colitis through suppressing Th1/17 mediated inflammation and promoting regulatory T cell response in interleukin-10 deficient mice
摘要拟观察CD52单克隆抗体对IL-10基因敲除克罗恩病模型小鼠结肠炎的治疗作用并揭示其可能的机制.结果显示,CD52单克隆抗体能有效治疗模型小鼠结肠炎症,降低Th1/17相关炎性因子的表达,同时能增加结肠固有层调节性T细胞的比例及功能.提示其治疗作用的机制可能与抑制Th1/17介导的炎症及诱导调节性T细胞反应相关.
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abstractsIn this study, we evaluated the therapeutic effects and possible mechanisms of anti-CD52 treatment on interleukin-10 (IL-10) deficient mice. Anti-mouse CD52 monoclonal antibody was administrated to C3H. IL-10-/-mice. The disease activity index, histological grading of colitis, serum Th1/17 related cytokines, percentage of CD25+Foxp3+T cells in colon as well as CD25, Foxp3 gene expression were measured. Our data suggested that anti-CD52 treatment inhibited colitis in C3H.IL-10-/-mice and it might be related to the suppression of Th1/17 related inflammation and the promotion of regulatory T cell differentiation.
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