MyD88 plays a critical T cell-intrinsic role in supporting CD8 T cell expansion during acute lymphocytic choriomeningitis virus infection.
MyD88 plays a critical T cell-intrinsic role in supporting CD8 T cell expansion during acute lymphocytic choriomeningitis virus infection.
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DOI：
10.4049/jimmunol.181.6.3804
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发表时间：
2008-09-15
期刊：
影响因子：
--
通讯作者：
Turka LA
中科院分区：
文献类型：
--
作者：
Rahman AH;Cui W;Larosa DF;Taylor DK;Zhang J;Goldstein DR;Wherry EJ;Kaech SM;Turka LA
在急性淋巴细胞性脉络丛脑膜炎病毒（LCMV）感染期间，CD8 T细胞迅速扩增并分化为病毒清除所需的效应子。在缺乏衔接分子MyD88的小鼠中，活化T细胞的积累大大减少。虽然MyD88通常被认为通过控制先天免疫细胞中炎性细胞因子的产生和Ag呈递来间接调节适应性免疫应答，但在这项研究中，我们确定了MyD88在LCMV特异性CD8 T细胞中的未被认识的细胞内在作用。使用相互过继转移模型和骨髓嵌合体，我们发现Myd 88 −/− CD8 T细胞在对LCMV感染的反应中克隆扩增有缺陷，与其环境无关。此外，我们表明，虽然MyD88在病毒感染的早期阶段对LCMV特异性CD8 T细胞的初始激活和分裂是不可或缺的，但MyD88依赖性信号对于支持它们的存活和持续积累至关重要。
During acute lymphocytic choriomeningitis virus (LCMV) infection, CD8 T cells rapidly expand and differentiate into effectors that are required for viral clearance. The accumulation of activated T cells is greatly reduced in mice lacking the adaptor molecule MyD88. Although MyD88 has generally been considered to indirectly regulate adaptive immune responses by controlling inflammatory cytokine production and Ag presentation in innate immune cells, in this study, we identify an unappreciated cell-intrinsic role for MyD88 in LCMV-specific CD8 T cells. Using reciprocal adoptive transfer models and bone marrow chimeras, we show that Myd88−/− CD8 T cells are defective in their clonal expansion in response to LCMV infection, independent of their environment. Furthermore, we show that while MyD88 is dispensable for initial activation and division of LCMV-specific CD8 T cells during the early stages of viral infection, MyD88-dependent signals are critical for supporting their survival and sustained accumulation.
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期刊：
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影响因子：
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