J. Exp. Med.
© The Rockefeller University Press
0022-1007/97/05/1777/07 $2.00
Volume 185, Number 10, May 19, 1997 1777-1783

A Regulatory Role for TRAF1 in Antigen-induced Apoptosis of  T Cells

By Daniel E. Speiser,^* Soo Young Lee,^§ Brian Wong,^§ Joseph Arron,^§ Angela Santana, Young-Yun Kong,^* Pamela S. Ohashi,^* and Yongwon Choi^§

From the ^* Ontario Cancer Institute, Departments of Medical Biophysics and Immunology, Toronto, Ontario M5G 2M9, Canada; and the  Howard Hughes Medical Institute and ^§ The Rockefeller University, New York 10021

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-B, 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.

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