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Regulation of the immune response by stress-activated protein kinases

published in: Immunological Reviews

date of publication: 2009-03-01

Cites articles 14

Date

Title

Authors

2006-10-01

Autophagy is induced in CD4+ T cells and important for the growth factor-withdrawal cell death
2006-02-01

The JNK are important for development and survival of macrophages

David A Hume, Timothy Ravasi
2006-11-01

Disruption of JNK2 decreases the cytokine response to Plasmodium falciparum glycosylphosphatidylinositol in vitro and confers protection in a cerebral malaria model

Michael Karin, Lena Serghides, Kevin C Kain
2006-04-01

Selective requirement of p38alpha MAPK in cytokine-dependent, but not antigen receptor-dependent, Th1 responses.
2006-07-01

ERK and p38 MAPK signaling pathways negatively regulate CIITA gene expression in dendritic cells and macrophages
2005-11-01

JNK1 is essential for CD8+ T cell-mediated tumor immune surveillance

Hongbo Chi, Richard Flavell, Roger John Davis
2005-02-01

MAPK p38 alpha is dispensable for lymphocyte development and proliferation.
2005-10-01

The death receptor Fas (CD95/APO-1) mediates the deletion of T lymphocytes undergoing homeostatic proliferation.

Karen A Fortner, Ralph C Budd
2004-12-01

Differential activation of ERK, p38, and JNK required for Th1 and Th2 deviation in myelin-reactive T cells induced by altered peptide ligand
2002-06-01

Murine Lyme arthritis development mediated by p38 mitogen-activated protein kinase activity

Erol Fikrig, Juan Anguita, Richard Flavell, Stephen W. Barthold, Roger John Davis
2001-03-01

A critical role for p38 mitogen-activated protein kinase in the maturation of human blood-derived dendritic cells induced by lipopolysaccharide, TNF-alpha, and contact sensitizers
2001-07

c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis
2000-09-01

JNK1 is required for T cell-mediated immunity against Leishmania major infection.

Richard Flavell, Roger John Davis
1997-02-01

Reprogramming the signalling requirement for AP-1 (activator protein-1) activation during differentiation of precursor CD4+ T-cells into effector Th1 and Th2 cells.

Richard Flavell, Roger John Davis, Mercedes Rincón

Article - wd:Q37416266

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