TRAF2 is essential for JNK but not NF-κB activation and regulates lymphocyte proliferation and survival

Soo Young Lee, Amy Reichlin, Angela Santana, Karen A. Sokol, Michel C. Nussenzweig, Yongwon Choi

Research output: Contribution to journalArticlepeer-review

402 Scopus citations

Abstract

TRAF2 is believed to mediate the activation of NF-κB and JNK induced by the tumor necrosis factor receptor (TNFR) superfamily, which elicits pleiotropic responses in lymphocytes. We have investigated the physiological roles of TRAF2 in these processes by expressing a lymphocyte-specific dominant negative form of TRAF2, thereby blocking this protein's effector function. We find that the TNFR superfamily signals require TRAF2 for activation of JNK but not NF-κB. In addition, we show that TRAF2 induces NF- κB-independent anti-apoptotic pathways during TNF-induced apoptosis. Inhibition of TRAF2 leads to splenomegaly, lymphadenopathy, and an increased number of B cells. These findings indicate that TRAF2 is involved in the regulation of lymphocyte function and growth in vivo.

Original languageEnglish
Pages (from-to)703-713
Number of pages11
JournalImmunity
Volume7
Issue number5
DOIs
StatePublished - Nov 1997

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