Rapid In Vivo Conversion of Effector T Cells into Th2 Cells during Helminth Infection
Rapid In Vivo Conversion of Effector T Cells into Th2 Cells during Helminth Infection
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DOI：
10.4049/jimmunol.1101164
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发表时间：
2012-01-15
影响因子：
4.4
通讯作者：
Voehringer, David
中科院分区：
文献类型：
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作者：
Panzer, Marc;Sitte, Selina;Voehringer, David
病原体、过敏原或自身抗原对免疫系统的刺激导致具有促炎或抗炎效应细胞功能的CD4(+) T细胞分化。根据功能特性以及特征细胞因子和转录因子的表达，效应CD4(+) T细胞主要分为Th1、Th2、Th17和调节性T(Treg)细胞。至少其中一些 T 细胞亚群仍然对外部信号有反应，并获得其他亚群的特性，这增加了利用这种功能可塑性用于治疗目的的希望。在这项研究中，我们使用Ag特异性过继转移模型，并确定体外极化或离体分离的Th1、Th17或Treg细胞是否可以通过感染胃肠蠕虫巴西圆线虫而在体内转化为表达IL-4的Th2细胞。 Th1 和 Th17 细胞可以重新极化以获得 IL-4 的表达，并分别失去其特征性细胞因子 IFN-γ 和 IL-17A 的表达。相比之下，体外产生的和离体分离的 Treg 细胞在很大程度上抵抗复极化。蠕虫诱导的 Th1 或 Th17 细胞向 Th2 细胞的转化可能部分解释了蠕虫感染与预防自身免疫性疾病之间的负相关性。免疫学杂志，2012，188：615-623。
Stimulation of the immune system by pathogens, allergens, or autoantigens leads to differentiation of CD4(+) T cells with pro- or anti-inflammatory effector cell functions. Based on functional properties and expression of characteristic cytokines and transcription factors, effector CD4(+) T cells have been grouped mainly into Th1, Th2, Th17, and regulatory T (Treg) cells. At least some of these T cell subsets remain responsive to external cues and acquire properties of other subsets, raising the hope that this functional plasticity might be exploited for therapeutic purposes. In this study, we used an Ag-specific adoptive transfer model and determined whether in vitro-polarized or ex vivo-isolated Th1, Th17, or Treg cells can be converted into IL-4-expressing Th2 cells in vivo by infection of mice with the gastrointestinal helminth Nippostrongylus brasiliensis. Th1 and Th17 cells could be repolarized to acquire the expression of IL-4 and lose the expression of their characteristic cytokines IFN-gamma and IL-17A, respectively. In contrast, both in vitro-generated and ex vivo-isolated Treg cells were largely resistant to repolarization. The helminth-induced conversion of Th1 or Th17 cells into Th2 cells may partially explain the inverse correlation between helminth infection and protection against autoimmune disorders. The Journal of Immunology, 2012, 188: 615-623.