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Articles

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.

¹Abbreviations used in this paper: GP, glycoprotein; LCMV, lymphocytic choriomeningitis virus; PI, propidium iodide; SEB, staphylococcal enterotoxin B; TNFR, tumor necrosis factor receptor.

The first two authors contributed equally to this report.

Pamela S. Ohashi and Yongwon Choi share senior authorship.

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