{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T17:11:26Z","timestamp":1791047486871,"version":"4.1.0"},"reference-count":57,"publisher":"Rockefeller University Press","issue":"7","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,4,1]]},"abstract":"<jats:p>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\u2212\/\u2212 mice showed a significantly lower virus-specific CD8+ T cell expansion. However, JNK1\u2212\/\u2212 mice cleared LCMV infection with similar kinetics as JNK+\/+ mice. Splenic T cells from LCMV-infected JNK1\u2212\/\u2212 animals produced interferon \u03b3 after stimulation with viral peptides. However, fewer JNK1\u2212\/\u2212 T cells acquired an activated phenotype (CD44hi) and more JNK1\u2212\/\u2212CD8+CD44hi cells underwent apoptosis than JNK+\/+ cells at the peak of the primary response. In contrast, LCMV-infected JNK2\u2212\/\u2212 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.<\/jats:p>","DOI":"10.1084\/jem.20011481","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:48:54Z","timestamp":1027702134000},"page":"801-810","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":68,"title":["c-Jun NH2-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8+ T Cell\u2013mediated Antiviral Immunity"],"prefix":"10.1084","volume":"195","author":[{"given":"Nathalie","family":"Arbour","sequence":"first","affiliation":[{"name":"1Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denise","family":"Naniche","sequence":"additional","affiliation":[{"name":"1Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dirk","family":"Homann","sequence":"additional","affiliation":[{"name":"1Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roger J.","family":"Davis","sequence":"additional","affiliation":[{"name":"2Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard A.","family":"Flavell","sequence":"additional","affiliation":[{"name":"3Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael B.A.","family":"Oldstone","sequence":"additional","affiliation":[{"name":"1Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2002,3,25]]},"reference":[{"key":"2023072511374365600_BIB1","doi-asserted-by":"crossref","first-page":"589","DOI":"10.1007\/s001090050063","volume":"74","year":"1996","journal-title":"J. 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