期刊
JOURNAL OF IMMUNOLOGY
卷 186, 期 1, 页码 143-155出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1000290
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资金
- American Heart Association
- National Institutes of Health [AI28847]
- Veterans Affairs
- Iowa Veterans Affairs Medical Center
- NATIONAL CANCER INSTITUTE [P30CA072720] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R56AI028847, R01AI028847, R29AI028847] Funding Source: NIH RePORTER
We recently reported that TNFR-associated factor (TRAF)3, a ubiquitously expressed adaptor protein, promotes mature B cell apoptosis. However, the specific function of TRAF3 in T cells has remained unclear. In this article, we report the generation and characterization of T cell-specific TRAF3(-/-) mice, in which the traf3 gene was deleted from thymocytes and T cells. Ablation of TRAF3 in the T cell lineage did not affect CD4 or CD8 T cell populations in secondary lymphoid organs or the numbers or proportions of CD4(+), CD8(+) or double-positive or double-negative thymocytes, except that the T cell-specific TRAF3(-/-) mice had a 2-fold increase in FoxP3(+) T cells. In striking contrast to mice lacking TRAF3 in B cells, the T cell TRAF3-deficient mice exhibited defective IgG1 responses to a T-dependent Ag, as well as impaired T cell-mediated immunity to infection with Listeria monocytogenes. Surprisingly, we found that TRAF3 was recruited to the TCR/CD28 signaling complex upon costimulation and that TCR/CD28-mediated proximal and distal signaling events were compromised by TRAF3 deficiency. These findings provide insights into the roles played by TRAF3 in T cell activation and T cell-mediated immunity. The Journal of Immunology, 2011, 186: 143-155.
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