The Journal of Experimental Medicine
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Published 25 March 2002. doi:10.1084/jem.20011481
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© Rockefeller University Press, 0022-1007/2002/4/801/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 7, April 1, 2002 801-810

Original Article

c-Jun NH2-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8+ T Cell–mediated Antiviral Immunity

Nathalie Arbour1, Denise Naniche1, Dirk Homann1, Roger J. Davis2, Richard A. Flavell3 and Michael B.A. Oldstone1

1 Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037
2 Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605
3 Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520

Address correspondence to Dr. Michael B.A. Oldstone, Division of Virology, Department of Neuropharmacology, The Scripps Research Institute (IMM-6), 10550 North Torrey Pines Rd., La Jolla, CA 92037. Phone: 858-784-8054; Fax: 858-784-9981; E-mail: mbaobo{at}scripps.edu

c-Jun NH2-terminal kinases (JNK) play important roles in T helper cell (Th) proliferation, differentiation, and maintenance of Th1/Th2 polarization. To determine whether JNKs are involved in antiviral T cell immunity, and whether JNK1 and JNK2 bear biological differences, we investigated the immune responses of JNK1-deficient and JNK2-deficient mice to lymphocytic choriomeningitis virus (LCMV). After LCMV infection, wild-type (JNK+/+) mice had a 5- to 10-fold increase in splenic CD8+ T cells. In contrast, infected JNK1-/- mice showed a significantly lower virus-specific CD8+ T cell expansion. However, JNK1-/- mice cleared LCMV infection with similar kinetics as JNK+/+ mice. Splenic T cells from LCMV-infected JNK1-/- animals produced interferon {gamma} after stimulation with viral peptides. However, fewer JNK1-/- T cells acquired an activated phenotype (CD44hi) and more JNK1-/-CD8+CD44hi cells underwent apoptosis than JNK+/+ cells at the peak of the primary response. In contrast, LCMV-infected JNK2-/- mice generated more virus-specific CD8+ T cells than JNK+/+ mice. These results indicate that JNK1 and JNK2 signal pathways have distinct roles in T cell responses during a viral infection. JNK1 is involved in survival of activated T cells during immune responses, and JNK2 plays a role in control of CD8+ T cell expansion in vivo.

Key Words: viral infection • cellular activation • T lymphocytes • protein kinases • lymphocytic choriomeningitis virus


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