Emerging Tim-3 functions in antimicrobial and tumor immunity.
Emerging Tim-3 functions in antimicrobial and tumor immunity.
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DOI：
10.1016/j.it.2011.05.003
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发表时间：
2011-08
影响因子：
16.8
通讯作者：
Kuchroo VK
中科院分区：
文献类型：
--
作者：
Sakuishi K;Jayaraman P;Behar SM;Anderson AC;Kuchroo VK
T细胞免疫球蛋白-3（Tim-3）被鉴定为分化的产生IFN-γ的CD 4 + T辅助1型和CD 8 + T细胞毒性1型细胞的标志物。Tim-3与其配体半乳糖凝集素-9（Gal-9）的相互作用诱导细胞死亡，并且这种相互作用的体内阻断导致实验模型中自身免疫性加剧和耐受性消除，从而确立Tim-3为负调节分子。最近的研究已经揭示了Tim-3负调节T细胞应答的其他机制，例如通过促进CD 8 + T细胞耗竭的发展和诱导髓源性抑制细胞（MDSC）的扩增。与这种对T细胞的抑制作用相反，Tim-3-Gal-9相互作用促进巨噬细胞清除细胞内病原体。在这里，我们将重点关注Tim-3在肿瘤和抗微生物免疫中的新作用。
T cell immunoglobulin-3 (Tim-3) was identified as a marker of differentiated IFN-γ-producing CD4+ T helper type 1 and CD8+ T cytotoxic type 1 cells. The interaction of Tim-3 with its ligand, galectin-9 (Gal-9), induces cell death and in vivo blockade of this interaction results in exacerbated autoimmunity and abrogation of tolerance in experimental models, establishing Tim-3 as a negative regulatory molecule. Recent studies have uncovered additional mechanisms by which Tim-3 negatively regulates T cell responses, such as by promoting the development of CD8+ T cell exhaustion and inducing expansion of myeloid-derived suppressor cells (MDSC). In contrast to this inhibitory effect on T cells, Tim-3-Gal-9 interaction promotes macrophage clearance of intracellular pathogens. Here, we will focus on the emerging role for Tim-3 in tumor and anti-microbial immunity.
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DOI：
10.1084/jem.20060210
发表时间：
2006-06-12
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Koguchi K;Anderson DE;Yang L;O'Connor KC;Kuchroo VK;Hafler DA
通讯作者：
Hafler DA
影响因子：
24.1
作者：
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影响因子：
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通讯作者：
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影响因子：
29.4
作者：
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通讯作者：
Bertoletti, Antonio
影响因子：
64.8
作者：
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通讯作者：
Walker, Bruce D.