中文摘要：

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—48h达到峰值，72h开始回落。进一步利用抗．CD25mAb7D4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Thl7的功能。进而抑制CHS的发生。

英文摘要：

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.