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【Nature Immunology 编译】TIM-1能诱导T细胞活化并且
TIM-1 induces T cell activation and inhibits the development of peripheral tolerance
来源
Nature Immunology 6, 447 - 454 (2005)
Published online: 27 March 2005; Corrected online: 30 March 2005 | doi:10.1038/ni1186
http://www.nature.com/ni/journal/v6/n5/abs/ni1186.html
摘要原文
We have examined the function of TIM-1, encoded by a gene identified as an 'atopy susceptibility gene' (Havcr1 *), and demonstrate here that TIM-1 is a molecule that costimulates T cell activation. TIM-1 was expressed on CD4+ T cells after activation and its expression was sustained preferentially in T helper type 2 (TH2) but not TH1 cells. In vitro stimulation of CD4+ T cells with a TIM-1-specific monoclonal antibody and T cell receptor ligation enhanced T cell proliferation; in TH2 cells, such costimulation greatly enhanced synthesis of interleukin 4 but not interferon-. In vivo, the use of antibody to TIM-1 plus antigen substantially increased production of both interleukin 4 and interferon- in unpolarized T cells, prevented the development of respiratory tolerance, and increased pulmonary inflammation. Our studies suggest that immunotherapies that regulate TIM-1 function may downmodulate allergic inflammatory diseases.
编译
TIM-1由一种叫“特应性基因”(Havcr1 *) 所编码。我们对其功能进行检测，发现TIM-1是一个可以共同刺激T细胞活化的的分子。TIM-1活化后表达在CD4+ T细胞，它在TH2辅助细胞表达的时间比TH1辅助细胞长。在体外用一种TIM-1特异的单克隆抗体刺激CD4+ T细胞，结果T细胞受体连接作用，增强了T细胞增殖。在TH2 辅助细胞，这种共同刺激极大的增强了白细胞介素4而不是γ干扰素的合成。在体内，用TIM-1抗体以及抗原刺激未极化的T细胞后，白细胞介素4和γ干扰素的合成都增加。阻止了呼吸耐受的发展，加重了肺部的炎症。我们的研究表明通过免疫疗法来调节TIM-1的功能可以下调过敏性的炎症疾病。 [标签:content1][标签:content2]
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作者:admin@医学,生命科学 2011-04-01 05:15
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