Th2细胞免疫反应在抗寄生虫感染和组织修复中有重要的作用，同时Th2细胞反应也可以引起慢性炎症反应如哮喘和过敏。Th2细胞分化的转录调控尽管研究了很多年，但仍有很多不清楚的地方。Id蛋白已报道参与调控很多细胞亚群的分化，但是否调控Th2细胞的分化没有任何报道。我们的前期结果显示，缺失Id2的CD4 T细胞，在体外培养和在体内诱导哮喘和巴西钩虫感染后，Th2细胞的分化严重缺陷。因此，本项目的目标是利用体外和体内系统，深入研究Th2细胞分化的调控网络，全面解析Id蛋白调控Th2细胞分化的分子机制。项目的研究对过敏性疾病及寄生虫感染的治疗和预防有重要意义。

T helper 2 (Th2) cells orchestrate protective type 2 immune responses, such as those that target helminths and facilitate tissue repair, but also contribute to chronic inflammatory diseases, such as asthma and allergy. Transcription regulation of Th2 cell differentiation has been study for many years, but how naive CD4 T cells commit to the T helper type 2 (Th2) lineage is remain poorly understood. Id protein has been showed to regulate different T helper subset, such as Th1, Treg, Th17 and Tfh differentiation. However, whether Id protein can regulate Th2 cell differentiation has never been studied. Here, by using Id2f/f/CD-Cre mice, our preliminary data indicated that Th2 cell response were strikingly impaired in CD4 T cells from Id2-deficient mice in vitro and in vivo in an asthma model and in response to parasitic nematode Nippostrongylus brasiliensis (Nb), a well-established model of migratory helminth infection. In this proposal, we aimed to study the molecular mechanism by which Id protein regulate Th2 cell differentiation and its implication in prevention or therapy of allergic disease and helminth infection.