| First Author | Nguyen LT | Year | 1999 |
| Journal | Immunity | Volume | 11 |
| Issue | 3 | Pages | 379-89 |
| PubMed ID | 10514016 | Mgi Jnum | J:57913 |
| Mgi Id | MGI:1346101 | Doi | 10.1016/s1074-7613(00)80113-2 |
| Citation | Nguyen LT, et al. (1999) TRAF2 deficiency results in hyperactivity of certain TNFR1 signals and impairment of CD40-mediated responses. Immunity 11(3):379-89 |
| abstractText | Tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2) can interact with various members of the TNF receptor family. Previously, we reported that TRAF2-deficient mice die prematurely and have elevated serum TNF levels. In this study, we demonstrate that TRAF2-deficient macrophages produce increased amounts of nitric oxide (NO) and TNF in response to TNF stimulation. Furthermore, we could enhance the survival of TRAF2-deficient mice by eliminating either TNF or TNFR1. Using these double-knockout mice, we show that in the absence of TRAF2, the T helper-dependent antibody response, CD40-mediated proliferation, and NF-kappaB activation are defective. These data demonstrate two important roles of TRAF2, one as a negative regulator of certain TNFR1 signals and the other as a positive mediator of CD40 signaling. |
