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The Non-Classical MAP Kinase ERK3 Controls T Cell Activation.

Marquis M, Boulet S, Mathien S, Rousseau J, Thébault P, Daudelin JF, Rooney J, Turgeon B, Beauchamp C, Meloche S, Labrecque N

Maisonneuve-Rosemont Hospital Research Centre, Montreal, Quebec, Canada ; Department of Microbiology, Infectiology and Immunology, University of Montreal, Quebec, Canada.

The classical mitogen-activated protein kinases (MAPKs) ERK1 and ERK2 are activated upon stimulation of cells with a broad range of extracellular signals (including antigens) allowing cellular responses to occur. ERK3 is an atypical member of the MAPK family with highest homology to ERK1/2. Therefore, we evaluated the role of ERK3 in mature T cell response. Mouse resting T cells do not transcribe ERK3 but its expression is induced in both CD4(+) and CD8(+) T cells following T cell receptor (TCR)-induced T cell activation. This induction of ERK3 expression in T lymphocytes requires activation of the classical MAPK ERK1 and ERK2. Moreover, ERK3 protein is phosphorylated and associates with MK5 in activated primary T cells. We show that ERK3-deficient T cells have a decreased proliferation rate and are impaired in cytokine secretion following in vitro stimulation with low dose of anti-CD3 antibodies. Our findings identify the atypical MAPK ERK3 as a new and important regulator of TCR-induced T cell activation.

PLoS ONE 2014;9(1):e86681.

Pubmed ID: 24475167

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