【进展|热点】曹雪涛Nature Immunology又发牛文！！！
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Nat Immunol. 2011 May;12(5):416-24. Epub 2011 Mar 27.
Intracellular MHC class II molecules promote TLR-triggered innate immune responses by maintaining activation of the kinase Btk
Liu X, Zhan Z, Li D, Xu L, Ma F, Zhang P, Yao H, Cao X.
Source National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China.
Abstract
The molecular mechanisms involved in the full activation of innate immunity achieved through Toll-like receptors (TLRs) remain to be fully elucidated. In addition to their classical antigen-presenting function, major histocompatibility complex (MHC) class II molecules might mediate reverse signaling. Here we report that deficiency in MHC class II attenuated the TLR-triggered production of proinflammatory cytokines and type I interferon in macrophages and dendritic cells, which protected mice from endotoxin shock. Intracellular MHC class II molecules interacted with the tyrosine kinase Btk via the costimulatory molecule CD40 and maintained Btk activation, but cell surface MHC class II molecules did not. Then, Btk interacted with the adaptor molecules MyD88 and TRIF and thereby promoted TLR signaling. Therefore, intracellular MHC class II molecules can act as adaptors, promoting full activation of TLR-triggered innate immune responses.
版主留言叫我写一点点评，我觉得文章的内容就不用说了，大家可以自己去看，我想说的是，在满天都是microRNA、Th17、Treg、Tfh、干细胞，唯恐自己落伍的今天，能把目光放在MHC这种古老分子上的人是有眼光的，有见解的，值得尊敬的，也必定是大师级的。从中我们能体会到作者免疫学研究的境界所在。
说的不对的大家指正。
Intracellular MHC class II molecules promote TLR-triggered innate immune responses by maintaining activation of the kinase Btk
Liu X, Zhan Z, Li D, Xu L, Ma F, Zhang P, Yao H, Cao X.
Source National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China.
Abstract
The molecular mechanisms involved in the full activation of innate immunity achieved through Toll-like receptors (TLRs) remain to be fully elucidated. In addition to their classical antigen-presenting function, major histocompatibility complex (MHC) class II molecules might mediate reverse signaling. Here we report that deficiency in MHC class II attenuated the TLR-triggered production of proinflammatory cytokines and type I interferon in macrophages and dendritic cells, which protected mice from endotoxin shock. Intracellular MHC class II molecules interacted with the tyrosine kinase Btk via the costimulatory molecule CD40 and maintained Btk activation, but cell surface MHC class II molecules did not. Then, Btk interacted with the adaptor molecules MyD88 and TRIF and thereby promoted TLR signaling. Therefore, intracellular MHC class II molecules can act as adaptors, promoting full activation of TLR-triggered innate immune responses.
版主留言叫我写一点点评，我觉得文章的内容就不用说了，大家可以自己去看，我想说的是，在满天都是microRNA、Th17、Treg、Tfh、干细胞，唯恐自己落伍的今天，能把目光放在MHC这种古老分子上的人是有眼光的，有见解的，值得尊敬的，也必定是大师级的。从中我们能体会到作者免疫学研究的境界所在。
说的不对的大家指正。
版主小舟儿留言:
如果能对文献内容做一个简要的介绍或评论，会有意外惊喜哦！
如果能对文献内容做一个简要的介绍或评论，会有意外惊喜哦！
