Development of Th1-type immune responses requires the type I cytokine receptor TCCR
Development of Th1-type immune responses requires the type I cytokine receptor TCCR
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DOI：
10.1038/35038103
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发表时间：
2000-10-19
期刊：
影响因子：
64.8
通讯作者：
de Sauvage, FJ
中科院分区：
文献类型：
--
作者：
Chen, Q;Ghilardi, N;de Sauvage, FJ
在抗原攻击时，辅助性T细胞分化成两个功能不同的亚群，Th 1和Th 2，其特征在于它们分泌的不同效应细胞因子（1）。Th 1细胞产生白细胞介素（IL）-2、干扰素-γ（IFN-γ）和α-光敏素-β，其介导对细胞介导的免疫应答的发展至关重要的促炎功能，而Th 2细胞分泌细胞因子，例如IL-4、IL-5和IL-10，其增强体液免疫（1，2）。辅助性T细胞分化的这一过程受到细胞因子的严格调控。在这里，我们报告的I型细胞因子受体家族的一个新成员，指定T细胞细胞因子受体（TCCR）。当在体内用蛋白质抗原攻击时，TCCR缺陷小鼠的Th 1应答受损，如通过IFN-γ产生所测量的。TCCR缺陷小鼠对细胞内病原体单核细胞增生李斯特菌感染的易感性也增加。此外，依赖于Th 1细胞的抗原特异性免疫球蛋白-γ 2a的水平在这些小鼠中显著降低。我们的研究结果表明，存在一种新的细胞因子受体参与调节适应性免疫反应和关键的Th 1反应的产生。
On antigen challenge, T-helper cells differentiate into two functionally distinct subsets, Th1 and Th2, characterized by the different effector cytokines that they secrete(1). Th1 cells produce interleukin (IL)-2, interferon-gamma (IFN-gamma) and lymphotoxin-beta, which mediate pro-inflammatory functions critical for the development of cell-mediated immune responses, whereas Th2 cells secrete cytokines such as IL-4, IL-5 and IL-10 that enhance humoral immunity(1,2). This process of T-helper cell differentiation is tightly regulated by cytokines. Here we report a new member of the type I cytokine receptor family, designated T-cell cytokine receptor (TCCR). When challenged in vivo with protein antigen, TCCR-deficient mice had impaired Th1 response as measured by IFN-gamma production. TCCR-deficient mice also had increased susceptibility to infection with an intracellular pathogen, Listeria monocytogenes. In addition, levels of antigen-specific immunoglobulin-gamma 2a, which are dependent on Th1 cells, were markedly reduced in these mice. Our results demonstrate the existence of a new cytokine receptor involved in regulating the adaptive immune response and critical to the generation of a Th1 response.