LPS-induced down-regulation of signal regulatory protein {alpha} contributes to innate immune activation in macrophages.

LPS-induced down-regulation of signal regulatory protein {alpha} contributes to innate immune activation in macrophages. Research Abstract Details 

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LPS-induced down-regulation of signal regulatory protein {alpha} contributes to innate immune activation in macrophages. Abstract Text:

Xiao-Ni Kong,He-Xin Yan,Lei Chen,Li-Wei Dong,Wen Yang,Qiong Liu,Le-Xing Yu,Dan-Dan Huang,Shu-Qin Liu,Hui Liu,Meng-Chao Wu,Hong-Yang Wang,Xiao-Ni Kong,He-Xin Yan,Lei Chen,Li-Wei Dong,Wen Yang,Qiong Liu,Le-Xing Yu,Dan-Dan Huang,Shu-Qin Liu,Hui Liu,Meng-Chao Wu,Hong-Yang Wang,

Activation of the mitogen-activated protein kinases (MAPKs) and nuclear factor kappaB (NF-kappaB) cascades after Toll-like receptor (TLR) stimulation contributes to innate immune responses. Signal regulatory protein (SIRP) alpha, a member of the SIRP family that is abundantly expressed in macrophages, has been implicated in regulating MAPK and NF-kappaB signaling pathways. In addition, SIRPalpha can negatively regulate the phagocytosis of host cells by macrophages, indicating an inhibitory role of SIRPalpha in innate immunity. We provide evidences that SIRPalpha is an essential endogenous regulator of the innate immune activation upon lipopolysaccharide (LPS) exposure. SIRPalpha expression was promptly reduced in macrophages after LPS stimulation. The decrease in SIRPalpha expression levels was required for initiation of LPS-induced innate immune responses because overexpression of SIRPalpha reduced macrophage responses to LPS. Knockdown of SIRPalpha caused prolonged activation of MAPKs and NF-kappaB pathways and augmented production of proinflammatory cytokines and type I interferon (IFN). Mice transferred with SIRPalpha-depleted macrophages were highly susceptible to endotoxic shock, developing multiple organ failure and exhibiting a remarkable increase in mortality. SIRPalpha may accomplish this mainly through its association and sequestration of the LPS signal transducer SHP-2. Thus, SIRPalpha functions as a biologically important modulator of TLR signaling and innate immunity.

LPS-induced down-regulation of signal regulatory protein {alpha} contributes to innate immune activation in macrophages. Publishing Authors By Initials

XN Kong,HX Yan,L Chen,LW Dong,W Yang,Q Liu,LX Yu,DD Huang,SQ Liu,H Liu,MC Wu,HY Wang,XN Kong,HX Yan,L Chen,LW Dong,W Yang,Q Liu,LX Yu,DD Huang,SQ Liu,H Liu,MC Wu,HY Wang,

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LPS-induced down-regulation of signal regulatory protein {alpha} contributes to innate immune activation in macrophages. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of experimental medicine

VOLUME: 204

Page Numbers: 2719-31

Journal Abbreviation: J. Exp. Med.

ISSN: 1540-9538

DAY: 22

MONTH: 10

YEAR: 2007

LPS-induced down-regulation of signal regulatory protein {alpha} contributes to innate immune activation in macrophages. Information

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LANGUAGE: eng

NlmUniqueID: 2985109

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Grant and Affiliation Information for LPS-induced down-regulation of signal regulatory protein {alpha} contributes to innate immune activation in macrophages.

AFFILIATION: International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai 200438, China.

Country: United States

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MEDLINETA: J Exp Med

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