期刊
IMMUNITY
卷 27, 期 2, 页码 253-267出版社
CELL PRESS
DOI: 10.1016/j.immuni.2007.07.012
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资金
- NCI NIH HHS [R01 CA099997-05, CA099997, R01 CA099997] Funding Source: Medline
- NIAID NIH HHS [R01 AI049993-07, R01 AI028847-16A1, AI28847, R56 AI049993, R01 AI049993, R01 AI028847-15, R01 AI028847, AI49993, R56 AI028847] Funding Source: Medline
Tumor necrosis factor receptor-associated factor 3 (TRAF3) is an adaptor protein that directly binds to a number of receptors of the tumor necrosis factor receptor (TNF-R) superfamily. Despite in vitro evidence that TRAF3 plays diverse roles in different cell types, little is known about the in vivo functions of TRAF3. To address this gap in knowledge and to circumvent the early lethal effect of TRAF3 null mutations, we generated conditional TRAF3-deficient mice. B-cell-specific Traf3(-/-) mice displayed severe peripheral B cell hyperplasia, which culminated in hyperimmunoglobulinemia. and increased T-independent antibody responses, splenomegaly and lymphadenopathy. Resting splenic B cells from these mice exhibited remarkably prolonged survival ex vivo independent of B cell activating factor and showed increased amounts of active nuclear factor-kappa B2 but decreased amounts of nuclear protein kinase C delta. Furthermore, these mice developed autoimmune manifestations as they aged. These findings indicate that TRAF3 is a critical regulator of peripheral B cell homeostasis and may be implicated in the regulation of peripheral self-tolerance induction.
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