Regulation of the immune response by stress-activated protein kinases

被引:224
作者
Rincon, Mercedes [1 ]
Davis, Roger J. [2 ,3 ]
机构
[1] Univ Vermont, Dept Med, Program Immunol, Burlington, VT 05405 USA
[2] Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA
[3] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA USA
关键词
B cells; dendritic cells; T cells; T-helper 1 (Th1); Th2; Th17; cells; cytotoxic T cells; autoimmunity; P38 MAP KINASE; JUN NH2-TERMINAL KINASE; T-CELL-ACTIVATION; N-TERMINAL KINASE; COLLAGEN-INDUCED ARTHRITIS; IFN-GAMMA PRODUCTION; C-JUN; DENDRITIC CELLS; GENE-EXPRESSION; IN-VIVO;
D O I
10.1111/j.1600-065X.2008.00744.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
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.
引用
收藏
页码:212 / 224
页数:13
相关论文
共 108 条
[1]
Essential role of p38α MAP kinase in placental but not embryonic cardiovascular development [J].
Adams, RH ;
Porras, A ;
Alonso, G ;
Jones, M ;
Vintersten, K ;
Panelli, S ;
Valladares, A ;
Perez, L ;
Klein, R ;
Nebreda, AR .
MOLECULAR CELL, 2000, 6 (01) :109-116
[2]
Activation of MAP kinase p38 is critical for the cell-cycle-controlled suppressor function of regulatory T cells [J].
Adler, Henric S. ;
Kubsch, Sebastian ;
Graulich, Edith ;
Ludwig, Stephan ;
Knop, Juergen ;
Steinbrink, Kerstin .
BLOOD, 2007, 109 (10) :4351-4359
[3]
Deficiency of the stress kinase p38α results in embryonic lethality:: Characterization of the kinase dependence of stress responses of enzyme-deficient embryonic stem cells [J].
Allen, M ;
Svensson, L ;
Roach, M ;
Hambor, J ;
McNeish, J ;
Gabel, CA .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 191 (05) :859-869
[4]
The kinases MSK1 and MSK2 act as negative regulators of Toll-like receptor signaling [J].
Ananieva, Olga ;
Darragh, Joanne ;
Johansen, Claus ;
Carr, Julia M. ;
McIlrath, Joanne ;
Park, Jin Mo ;
Wingate, Andrew ;
Monk, Claire E. ;
Toth, Rachel ;
Santos, Susana G. ;
Iversen, Lars ;
Arthur, J. Simon C. .
NATURE IMMUNOLOGY, 2008, 9 (09) :1028-1036
[5]
Murine Lyme arthritis development mediated by p38 mitogen-activated protein kinase activity [J].
Anguita, J ;
Barthold, SW ;
Persinski, R ;
Hedrick, MN ;
Huy, CA ;
Davis, RJ ;
Flavell, RA ;
Fikrig, E .
JOURNAL OF IMMUNOLOGY, 2002, 168 (12) :6352-6357
[6]
c-Jun NH2-terminal kinase (JNK)1 and JNK2 signaling pathways have divergent roles in CD8+ T cell-mediated antiviral immunity [J].
Arbour, N ;
Naniche, D ;
Homann, D ;
Davis, RJ ;
Flavell, RA ;
Oldstone, MBA .
JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 195 (07) :801-810
[7]
A critical pole for p38 mitogen-activated protein kinase in the maturation of human blood-derived dendritic cells induced by lipopolysaccharide, TNF-α, and contact sensitizers [J].
Arrighi, JF ;
Rebsamen, M ;
Rousset, F ;
Kindler, V ;
Hauser, C .
JOURNAL OF IMMUNOLOGY, 2001, 166 (06) :3837-3845
[8]
The many paths to p38 mitogen-activated protein kinase activation in the immune system [J].
Ashwell, Jonathan D. .
NATURE REVIEWS IMMUNOLOGY, 2006, 6 (07) :532-540
[9]
Generation and characterization of p38β (MAPK11) gene-targeted mice [J].
Beardmore, VA ;
Hinton, HJ ;
Eftychi, C ;
Apostolaki, M ;
Armaka, M ;
Darragh, J ;
McIlrath, J ;
Carr, JM ;
Armit, LJ ;
Clacher, C ;
Malone, L ;
Kollias, G ;
Arthur, JSC .
MOLECULAR AND CELLULAR BIOLOGY, 2005, 25 (23) :10454-10464
[10]
Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of activated T cell (NF-AT) [J].
Behrens, A ;
Sabapathy, K ;
Graef, I ;
Cleary, M ;
Crabtree, GR ;
Wagner, EF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (04) :1769-1774