A regulatory role for TRAF1 in antigen-induced apoptosis of T cells

Details

Serval ID
serval:BIB_56AA7436F9BC
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
A regulatory role for TRAF1 in antigen-induced apoptosis of T cells
Journal
Journal of Experimental Medicine
Author(s)
Speiser  D. E., Lee  S. Y., Wong  B., Arron  J., Santana  A., Kong  Y. Y., Ohashi  P. S., Choi  Y.
ISSN
0022-1007 (Print)
Publication state
Published
Issued date
05/1997
Volume
185
Number
10
Pages
1777-83
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: May 19
Abstract
Tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2) and TRAF1 were found as components of the TNFR2 signaling complex, which exerts multiple biological effects on cells such as cell proliferation, cytokine production, and cell death. In the TNFR2-mediated signaling pathways, TRAF2 works as a mediator for activation signals such as NF-kappaB, but the role of TRAF1 has not been previously determined. Here we show in transgenic mice that TRAF1 overexpression inhibits antigen-induced apoptosis of CD8(+) T lymphocytes. Our results demonstrate a biological role for TRAF1 as a regulator of apoptotic signals and also support the hypothesis that the combination of TRAF proteins in a given cell type determines distinct biological effects triggered by members of the TNF receptor superfamily.
Keywords
Animals Antigens *Apoptosis CD8-Positive T-Lymphocytes/immunology Cell Survival Cytotoxicity, Immunologic Lymph Nodes/immunology Lymphocyte Activation Macrophages/immunology Mice Mice, Transgenic Proteins/genetics/*physiology Receptors, Antigen, T-Cell, alpha-beta/genetics/*physiology Receptors, Tumor Necrosis Factor/physiology Recombinant Fusion Proteins/biosynthesis Signal Transduction Spleen/immunology T-Lymphocytes/cytology/immunology/*physiology TNF Receptor-Associated Factor 1 TNF Receptor-Associated Factor 2
Pubmed
Web of science
Open Access
Yes
Create date
28/01/2008 11:33
Last modification date
20/08/2019 14:10
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