Sheng Xu;Xingguang Liu;Yan Bao;Xuhui Zhu;Chaofeng Han;Peng Zhang;Xuemin Zhang;Weihua Li;雪涛 曹
Second Military Medical University;National Center of Biomedical Analysis;China Association for Science and Technology
发表时间:2012-6
期 刊:Nature Immunology
语 言:English
U R L: http://www.scopus.com/inward/record.url?scp=84861233283&partnerID=8YFLogxK
The molecular mechanisms that fine-tune Toll-like receptor (TLR)-triggered innate inflammatory responses remain to be fully elucidated. Major histocompatibility complex (MHC) molecules can mediate reverse signaling and have nonclassical functions. Here we found that constitutively expressed membrane MHC class I molecules attenuated TLR-triggered innate inflammatory responses via reverse signaling, which protected mice from sepsis. The intracellular domain of MHC class I molecules was phosphorylated by the kinase Src after TLR activation, then the tyrosine kinase Fps was recruited via its Src homology 2 domain to phosphorylated MHC class I molecules. This led to enhanced Fps activity and recruitment of the phosphatase SHP-2, which interfered with TLR signaling mediated by the signaling molecule TRAF6. Thus, constitutive MHC class I molecules engage in crosstalk with TLR signaling via the Fps-SHP-2 pathway and control TLR-triggered innate inflammatory responses.
医学与生命科学
Scopus度量
年份 | CiteScore | SJR | SNIP |
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1996 | |||
1997 | |||
1998 | |||
1999 | |||
2000 | |||
2001 | 8.961 | 2.486 | |
2002 | 14.426 | 3.696 | |
2003 | 15.02 | 3.712 | |
2004 | 17.013 | 3.915 | |
2005 | 17.93 | 3.691 | |
2006 | 20.283 | 4.13 | |
2007 | 20.217 | 3.882 | |
2008 | 19.372 | 3.578 | |
2009 | 17.635 | 3.104 | |
2010 | 18.629 | 3.084 | |
2011 | 37.4 | 18.437 | 3.915 |
2012 | 41.4 | 18.857 | 4.139 |
2013 | 43.9 | 15.038 | 5.102 |
2014 | 38 | 14.632 | 3.964 |
2015 | 34.4 | 11.699 | 3.748 |
2016 | 33.2 | 15.21 | 3.949 |
2017 | 35.4 | 14.007 | 4.03 |
2018 | 36.5 | 13.3 | 4.409 |
2019 | 29 | 9.283 | 3.703 |
2020 | 25.7 | ||
2021 |
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