Published 25 March 2002. doi:10.1084/jem.20011508
© Rockefeller University Press, 0022-1007/2002/4/811/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 7, April 1, 2002 811-823
c-Jun NH2-Terminal Kinase (JNK)1 and JNK2 Have Distinct Roles in CD8+ T Cell Activation
Dietrich Conze1,
Troy Krahl1,
Norman Kennedy3,
Linda Weiss1,
Joanne Lumsden2,
Patricia Hess3,
Richard A. Flavell4,
Graham Le Gros2,
Roger J. Davis3 and
Mercedes Rincón1
1 Section of Immunobiology, Department of Medicine, University of Vermont, Burlington, VT 05405
2 Malaghan Institute of Medical Research, Wellington School of Medicine, 6002 Wellington, New Zealand
3 Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School and Howard Hughes Medical Institute, Worcester, MA 01605
4 Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520
Address correspondence to Mercedes Rincón, Section of Immunology/Department of Medicine, D-305, Given Building, University of Vermont, Burlington, VT 05405. Phone: 802-656-0937; Fax: 802-656-3854; E-mail: mrincon{at}zoo.uvm.edu
The c-Jun NH2-terminal kinase (JNK) signaling pathway is induced by cytokines and stress stimuli and is implicated in cell death and differentiation, but the specific function of this pathway depends on the cell type. Here we examined the role of JNK1 and JNK2 in CD8+ T cells. Unlike CD4+ T cells, the absence of JNK2 causes increased interleukin (IL)-2 production and proliferation of CD8+ T cells. In contrast, JNK1-deficient CD8+ T cells are unable to undergo antigen-stimulated expansion in vitro, even in the presence of exogenous IL-2. The hypoproliferation of these cells is associated with impaired IL-2 receptor
chain (CD25) gene and cell surface expression. The reduced level of nuclear activating protein 1 (AP-1) complexes in activated JNK1-deficient CD8+ T cells can account for the impaired IL-2 receptor
chain gene expression. Thus, JNK1 and JNK2 play different roles during CD8+ T cell activation and these roles differ from those in CD4+ T cells.
Key Words: T lymphocytes MAP kinases IL-2R
AP-1 c-Jun

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