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作 者:王庆辉[1] 冯永辉[1] 刘军[1] 李莹[2] 曹雅明[1] 吕昌龙[1]
机构地区:[1]中国医科大学基础医学院免疫学教研室,辽宁沈阳110001 [2]沈阳市胸科医院检验科,辽宁沈阳110044
出 处:《微生物学杂志》2012年第6期65-68,共4页Journal of Microbiology
基 金:国家自然科学基金(30901343)
摘 要:接触性超敏反应(CHS)是研究体内免疫活化和调节的重要模型之一。分泌IL-17的CD4+Th(Th17)细胞亚群在CHS发展过程中发挥重要作用。CD4+CD25+FoxP3+调节性T细胞(Treg)是具有较强免疫调控作用的T细胞亚群。在氯化苦咪酸(TNCB)诱导的接触性超敏反应小鼠模型中,TNCB攻击后小鼠Treg占CD4+T细胞的百分比显著增高,于24~48 h达到峰值,72 h开始回落。进一步利用抗-CD25 mAb 7D4在小鼠体内消除Treg后,小鼠的受攻击皮肤增厚明显高于对照组。尽管CD4+T细胞在淋巴细胞中总的比例没有显著变化,但CD4+IL-17+T细胞比例显著增加。由此提示,CD4+CD25+FoxP3+Treg可能通过影响效应性Th17的功能,进而抑制CHS的发生。Contact hypersensitivity (CHS) was one of the most intensively studied in vivo models of immune activation and the regulation. IL-17 producing CD4 + T helper (Th17) subset played an important role in the pathogenesis of contact hypersensitivity. CD4+ CD25 + FoxP3 + regulatory T cells (Trcg) act as T subset with immunoregulatory function. In the trinitrochlorobenzene (TNCB) induced contact hypersensitivity model, the percentage of Trcg in CD4 * cells significantly increased following TNCB challenge, peaked at 24 +48 h, and then fell at 72h. After deple- tion of Treg with injection of anti-CD25 mAb (71)4) into mice, compared with control group, ear swelling was significantly higher in Treg-depleted group. In agreement, the percentage of IL-17 producing CD4 +T was also enhanced followed by Trcg depletion, although the ration of CD4 + T remains. These data suggested that CD4 + CD25 + FoxP3 + Treg suppress the Clt$ possibly via influencing the function of Thl7.
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