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c-Jun NH(2)-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8(+) T Cell–mediated Antiviral Immunity

c-Jun NH(2)-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 immun...

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Autores principales: Arbour, Nathalie, Naniche, Denise, Homann, Dirk, Davis, Roger J., Flavell, Richard A., Oldstone, Michael B.A.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2002
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193720/
https://www.ncbi.nlm.nih.gov/pubmed/11927625
http://dx.doi.org/10.1084/jem.20011481
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author Arbour, Nathalie
Naniche, Denise
Homann, Dirk
Davis, Roger J.
Flavell, Richard A.
Oldstone, Michael B.A.
author_facet Arbour, Nathalie
Naniche, Denise
Homann, Dirk
Davis, Roger J.
Flavell, Richard A.
Oldstone, Michael B.A.
author_sort Arbour, Nathalie
collection PubMed
description c-Jun NH(2)-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 γ after stimulation with viral peptides. However, fewer JNK1(−/−) T cells acquired an activated phenotype (CD44(hi)) and more JNK1(−/−)CD8(+)CD44(hi) 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.
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spelling pubmed-21937202008-04-14 c-Jun NH(2)-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8(+) T Cell–mediated Antiviral Immunity Arbour, Nathalie Naniche, Denise Homann, Dirk Davis, Roger J. Flavell, Richard A. Oldstone, Michael B.A. J Exp Med Original Article c-Jun NH(2)-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 γ after stimulation with viral peptides. However, fewer JNK1(−/−) T cells acquired an activated phenotype (CD44(hi)) and more JNK1(−/−)CD8(+)CD44(hi) 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. The Rockefeller University Press 2002-04-01 /pmc/articles/PMC2193720/ /pubmed/11927625 http://dx.doi.org/10.1084/jem.20011481 Text en Copyright © 2002, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Original Article
Arbour, Nathalie
Naniche, Denise
Homann, Dirk
Davis, Roger J.
Flavell, Richard A.
Oldstone, Michael B.A.
c-Jun NH(2)-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8(+) T Cell–mediated Antiviral Immunity
title c-Jun NH(2)-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8(+) T Cell–mediated Antiviral Immunity
title_full c-Jun NH(2)-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8(+) T Cell–mediated Antiviral Immunity
title_fullStr c-Jun NH(2)-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8(+) T Cell–mediated Antiviral Immunity
title_full_unstemmed c-Jun NH(2)-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8(+) T Cell–mediated Antiviral Immunity
title_short c-Jun NH(2)-Terminal Kinase (JNK)1 and JNK2 Signaling Pathways Have Divergent Roles in CD8(+) T Cell–mediated Antiviral Immunity
title_sort c-jun nh(2)-terminal kinase (jnk)1 and jnk2 signaling pathways have divergent roles in cd8(+) t cell–mediated antiviral immunity
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193720/
https://www.ncbi.nlm.nih.gov/pubmed/11927625
http://dx.doi.org/10.1084/jem.20011481
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