Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways

T helper type 1 cells (Th1) become anergic when stimulated through the antigen receptor in the absence of costimulation. They do not produce IL-2 or proliferate in response to subsequent stimulation. Previous studies have indicated that anergic T cells are defective in the trnsactivational activity...

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Format: Online
Language:English
Published: The Rockefeller University Press 1996
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192566/
id pubmed-2192566
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spelling pubmed-21925662008-04-16 Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways Articles T helper type 1 cells (Th1) become anergic when stimulated through the antigen receptor in the absence of costimulation. They do not produce IL-2 or proliferate in response to subsequent stimulation. Previous studies have indicated that anergic T cells are defective in the trnsactivational activity of the transcription factor, AP-1, which is required for optimal IL-2 transcription. Using two murine Th1 cell clones, we demonstrate that anergic Th1 cells have defects in both jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) activities. These kinases have been shown to be important for the upregulation of AP-1 activity. Furthermore, our data show that ERK and JNK activities are restored when anergy is induced in the presence of the protein synthesis inhibitor cycloheximide, or when anergic T cells are allowed to proliferate in response to exogenous IL-2. These treatments have previously been shown to prevent or reverse the anergic state. Our results suggest that defects in both JNK and ERK may result in the decreased AP-1 activity and the reduced IL-2 transcription observed in anergic T cells. The Rockefeller University Press 1996-05-01 /pmc/articles/PMC2192566/ /pubmed/8642312 Text en 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/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
title Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways
spellingShingle Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways
title_short Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways
title_full Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways
title_fullStr Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways
title_full_unstemmed Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways
title_sort anergic t cells are defective in both jun nh2-terminal kinase and mitogen-activated protein kinase signaling pathways
description T helper type 1 cells (Th1) become anergic when stimulated through the antigen receptor in the absence of costimulation. They do not produce IL-2 or proliferate in response to subsequent stimulation. Previous studies have indicated that anergic T cells are defective in the trnsactivational activity of the transcription factor, AP-1, which is required for optimal IL-2 transcription. Using two murine Th1 cell clones, we demonstrate that anergic Th1 cells have defects in both jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) activities. These kinases have been shown to be important for the upregulation of AP-1 activity. Furthermore, our data show that ERK and JNK activities are restored when anergy is induced in the presence of the protein synthesis inhibitor cycloheximide, or when anergic T cells are allowed to proliferate in response to exogenous IL-2. These treatments have previously been shown to prevent or reverse the anergic state. Our results suggest that defects in both JNK and ERK may result in the decreased AP-1 activity and the reduced IL-2 transcription observed in anergic T cells.
publisher The Rockefeller University Press
publishDate 1996
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192566/
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