NDLI: In vivo anergized CD4+ T cells express perturbed AP-1 and NF-kappa B transcription factors.

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In vivo anergized CD4+ T cells express perturbed AP-1 and NF-kappa B transcription factors.

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In vivo anergized CD4+ T cells express perturbed AP-1 and NF-kappa B transcription factors.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Leanderson, T. Dohlsten, M. Hedlund, G. Sundstedt, A. Sigvardsson, M. Kalland, T.
Description	Author Affiliation: Sundstedt A ( Pharmacia Oncology Immunology, Lund, Sweden.);
Abstract	Anergy is a major mechanism to ensure antigen-specific tolerance in T lymphocytes in the adult. In vivo, anergy has mainly been studied at the cellular level. In this study, we used the T-cell-activating superantigen staphylococcal enterotoxin A (SEA) to investigate molecular mechanisms of T-lymphocyte anergy in vivo. Injection of SEA to adult mice activates CD4+ T cells expressing certain T-cell receptor (TCR) variable region beta-chain families and induces strong and rapid production of interleukin 2 (IL-2). In contrast, repeated injections of SEA cause CD4+ T-cell deletion and anergy in the remaining CD4+ T cells, characterized by reduced expression of IL-2 at mRNA and protein levels. We analyzed expression of AP-1, NF-kappa B, NF-AT, and octamer binding transcription factors, which are known to be involved in the regulation of IL-2 gene promoter activity. Large amounts of AP-1 and NF-kappa B and significant quantities of NF-AT were induced in SEA-activated CD4+ spleen T cells, whereas Oct-1 and Oct-2 DNA binding activity was similar in both resting and activated T cells. In contrast, anergic CD4+ T cells contained severely reduced levels of AP-1 and Fos/Jun-containing NF-AT complexes but expressed significant amounts of NF-kappa B and Oct binding proteins after SEA stimulation. Resolution of the NF-kappa B complex demonstrated predominant expression of p50-p65 heterodimers in activated CD4+ T cells, while anergic cells mainly expressed the transcriptionally inactive p50 homodimer. These alterations of transcription factors are likely to be responsible for repression of IL-2 in anergic T cells.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	3
Volume Number	93
Language	English
Publisher	National Academy of Sciences
Publisher Date	1996-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	CD4-Positive T-Lymphocytes Immunology Metabolism Clonal Anergy Gene Expression NF-kappa B Biosynthesis Transcription Factor AP-1 Animals Binding Sites Drug Effects Cell Nucleus Enterotoxins Pharmacology Gene Expression Regulation Interferon Inducers Interleukin-2 Genetics Lymphocyte Activation Mice Mice, Inbred C57BL Mice, Transgenic Molecular Sequence Data Oligodeoxyribonucleotides Promoter Regions, Genetic Receptors, Antigen, T-Cell, Alpha-beta Superantigens Transcription Factors Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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