MHC class II-dependent basophil-CD4+ T cell interactions promote T(H)2 cytokine-dependent immunity.

MHC class II-dependent basophil-CD4+ T cell interactions promote T(H)2 cytokine-dependent immunity.
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DOI:
10.1038/ni.1740
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发表时间:
2009-07
期刊:
影响因子:
30.5
通讯作者:
--
中科院分区:
医学1区
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--
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树突状细胞可以引发幼稚的CD 4 + T细胞,然而,我们证明DC介导的引发不足以发展TH 2细胞依赖性免疫。我们确定嗜碱性粒细胞作为一个占主导地位的细胞群体,共表达MHC II类和IL 4的消息蠕虫感染后。胸腺基质淋巴细胞生成素(TSLP)促进嗜碱性粒细胞增多,嗜碱性粒细胞耗竭损害对蠕虫感染的免疫力。在体外,嗜碱性粒细胞促进抗原特异性CD 4 + T细胞增殖和IL-4的产生和嗜碱性粒细胞的转移增强蠕虫反应性CD 4 + T细胞在体内的扩增。总的来说,这些研究表明,MHC II类依赖嗜碱性粒细胞和CD 4 + T细胞之间的相互作用,促进TH 2细胞因子的反应和免疫力对蠕虫感染。
Dendritic cells can prime naïve CD4+ T cells, however we demonstrate that DC-mediated priming is insufficient for the development of TH2 cell-dependent immunity. We identify basophils as a dominant cell population that coexpressed MHC class II and Il4 message following helminth infection. Basophilia was promoted by thymic stromal lymphopoietin (TSLP) and depletion of basophils impaired immunity to helminth infection. In vitro, basophils promoted antigen-specific CD4+ T cell proliferation and IL-4 production and transfer of basophils augmented the expansion of helminth-responsive CD4+ T cells in vivo. Collectively, these studies suggest that MHC class II-dependent interactions between basophils and CD4+ T cells promote TH2 cytokine responses and immunity against helminth infection.
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