SOCS proteins in infectious diseases of mammals

被引：47

作者：

Delgado-Ortega, Mario ^{[1
,2
]}

Marc, Daniel ^{[1
,2
]}

Dupont, Joelle ^{[3
]}

Trapp, Sascha ^{[1
,2
]}

Berri, Mustapha ^{[1
,2
]}

Meurens, Francois ^{[4
]}

机构：

[1] INRA, Infectiol & Sante Publ UMR1282, F-37380 Nouzilly, France

[2] Univ Tours, Infectiol & Sante Publ UMR1282, F-37000 Tours, France

[3] INRA, Physiol Reprod & Comportements UMR85, F-37380 Nouzilly, France

[4] Univ Saskatchewan, Vaccine & Infect Dis Org InterVac, Saskatoon, SK S7N 5E3, Canada

来源：

VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY | 2013年 / 151卷 / 1-2期

关键词：

CIS; SOCS; Infectious diseases; Cytokines; Mammals; RESPIRATORY SYNCYTIAL VIRUS; CYTOKINE SIGNALING SOCS; STAT INHIBITOR-1 (SSI-1)/SUPPRESSOR; JANUS TYROSINE KINASE; T-CELL RESPONSES; MESSENGER-RNA; ANTIGEN PRESENTATION; NEGATIVE REGULATION; IMMUNE-RESPONSES; INSULIN-RECEPTOR;

D O I：

10.1016/j.vetimm.2012.11.008

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

As for most biological processes, the immune response to microbial infections has to be tightly controlled to remain beneficial for the host. Inflammation is one of the major consequences of the host's immune response. For its orchestration, this process requires a fine-tuned interplay between interleukins, endothelial cells and various types of recruited immune cells. Suppressors of cytokine signalling (SOCS) proteins are crucially involved in the complex control of the inflammatory response through their actions on various signalling pathways including the JAK/STAT and NF-kappa B pathways. Due to their cytokine regulatory functions, they are frequent targets for exploitation by infectious agents trying to escape the host's immune response. This review article aims to summarize our current knowledge regarding SOCS family members in the different mammalian species studied so far, and to display their complex molecular interactions with microbial pathogens. (C) 2012 Elsevier B.V. All rights reserved.

引用

页码：1 / 19

页数：19

共 166 条

[1] Enhancement of Antiviral Immunity by Small Molecule Antagonist of Suppressor of Cytokine Signaling [J].