TRAF2 Deficiency Results in Hyperactivity of Certain TNFR1 Signals and Impairment of CD40-Mediated Responses
Copyright policy )TRAF2 Deficiency Results in Hyperactivity of Certain TNFR1 Signals and Impairment of CD40-Mediated Responses
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.
- Amgen (Canada) Canada
- University of Toronto Canada
- Ludwig Institute for Cancer Research United States
- Ludwig Cancer Research Belgium
- University Hospital of Lausanne Switzerland
Male, Immunology, Nitric Oxide Synthase Type II, Nitric Oxide, Mice, Antigens, CD, Immunology and Allergy, Animals, CD40 Antigens, Cells, Cultured, Mice, Knockout, Mice, Inbred BALB C, NF-kappa B, Immunoglobulin Class Switching, Interleukin-12, Immunoglobulin Isotypes, Mice, Inbred C57BL, Infectious Diseases, Phenotype, Macrophages, Peritoneal, Female, Nitric Oxide Synthase, Cell Division
Male, Immunology, Nitric Oxide Synthase Type II, Nitric Oxide, Mice, Antigens, CD, Immunology and Allergy, Animals, CD40 Antigens, Cells, Cultured, Mice, Knockout, Mice, Inbred BALB C, NF-kappa B, Immunoglobulin Class Switching, Interleukin-12, Immunoglobulin Isotypes, Mice, Inbred C57BL, Infectious Diseases, Phenotype, Macrophages, Peritoneal, Female, Nitric Oxide Synthase, Cell Division
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