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PMID: 1509265 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Transactivation by AP-1 is a molecular target of T cell clonal anergy.

Science (New York, N.Y.) ·Vol. 257 ·No. 5073 ·1992-08-21 ·Pages 1134-8

Kang SM, Beverly B, Tran AC, Brorson K, Schwartz RH, Lenardo MJ

Abstract

Anergy is a mechanism of T lymphocyte tolerance induced by antigen receptor stimulation in the absence of co-stimulation. Anergic T cells were shown to have a defect in antigen-induced transcription of the interleukin-2 gene. Analysis of the promoter indicated that the transcription factor AP-1 and its corresponding cis element were specifically down-regulated. Exposure of anergic T cells to interleukin-2 restored both antigen responsiveness and activity of the AP-1 element.

MeSH Terms
Animals Antigen-Presenting Cells/immunology Antigens/immunology Base Sequence Binding Sites Blotting, Northern Cell Line Concanavalin A/pharmacology Gene Expression Regulation Immune Tolerance Interleukin-2/genetics,pharmacology Mice Molecular Sequence Data Mutation Promoter Regions, Genetic/genetics Proto-Oncogene Proteins c-jun/physiology RNA, Messenger/metabolism Receptors, Antigen, T-Cell/immunology T-Lymphocytes/immunology Transcription, Genetic Transfection
Chemicals
Antigens Interleukin-2 Proto-Oncogene Proteins c-jun RNA, Messenger Receptors, Antigen, T-Cell Concanavalin A
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Kang S M
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Beverly B
Tran A C
Brorson K
Schwartz R H
Lenardo M J
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
0036-8075
Published
1992-08-21
Pages
1134-8
Language
English
Region
United States
NLM ID
0404511
Subset
IM
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