Regulation of the immune response by stress‐activated protein kinases
- 6 March 2009
- journal article
- review article
- Published by Wiley in Immunological Reviews
- Vol. 228 (1) , 212-224
- https://doi.org/10.1111/j.1600-065x.2008.00744.x
Abstract
Activation of immune cells to mediate an immune response is often triggered by potential 'danger' or 'stress' stimuli that the organism receives. Within the mitogen-activated protein kinases (MAPKs) family, the stress-activated protein kinase (SAPK) group was defined as group of kinases that activated by stimuli that cause cell stress. In the immune cells, SAPKs are activated by antigen receptors (B- or T-cell receptors), Toll-like receptors, cytokine receptors, and physical-chemical changes in the environment among other stimuli. The SAPKs are established to be important mediators of intracellular signaling during adaptive and innate immune responses. Here we summarize what is currently known about the role of two sub-groups of SAPKs - c-Jun NH(2)-terminal kinase and p38 MAPK-in the function of specific components of the immune system and the overall contribution to the immune response.Keywords
This publication has 109 references indexed in Scilit:
- Human Immunodeficiency Virus Type 1 Nef Induces Programmed Death 1 Expression through a p38 Mitogen-Activated Protein Kinase-Dependent MechanismJournal of Virology, 2008
- The kinase p38α serves cell type–specific inflammatory functions in skin injury and coordinates pro- and anti-inflammatory gene expressionNature Immunology, 2008
- Phosphorylation by p38 MAPK as an Alternative Pathway for GSK3β InactivationScience, 2008
- Histamine receptor H1 is required for TCR-mediated p38 MAPK activation and optimal IFN-γ production in miceJournal of Clinical Investigation, 2007
- c-Jun N-Terminal Kinase 1 Is Required for Toll-Like Receptor 1 Gene Expression in MacrophagesInfection and Immunity, 2007
- p38α suppresses normal and cancer cell proliferation by antagonizing the JNK–c-Jun pathwayNature Genetics, 2007
- Inactivation of JNK1 enhances innate IL-10 production and dampens autoimmune inflammation in the brainProceedings of the National Academy of Sciences, 2006
- p38γ regulates the localisation of SAP97 in the cytoskeleton by modulating its interaction with GKAPThe EMBO Journal, 2005
- Activation and signaling of the p38 MAP kinase pathwayCell Research, 2005
- p38 MAP kinases: key signalling molecules as therapeutic targets for inflammatory diseasesNature Reviews Drug Discovery, 2003