期刊
TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE
卷 236, 期 2, 页码 139-154出版社
TOHOKU UNIV MEDICAL PRESS
DOI: 10.1620/tjem.236.139
关键词
CD4(+) T cells; signalosome; T-cell biology; TNFR; TRAF
资金
- Japan Society for the Promotion of Science [24590571]
- Ichiro Kanehara Foundation
- Takeda Science Foundation
- Suzuken Memorial Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Astellas Foundation for Research on Metabolic Disorders
- Waksman Foundation of Japan INC
- SENSHIN Medical Research Foundation
- Grants-in-Aid for Scientific Research [15H04640, 15H04742, 24590571] Funding Source: KAKEN
CD4(+) T helper cells (T-H cells), such as T(H)1, T(H)2, T(H)17, T-FH, and T-reg cells, play critical roles in host defense against infection and in the pathogenesis of immune-mediated diseases. Antigen-presenting cells, such as dendritic cells, deliver three kinds of signals essential for the activation, differentiation, and survival of naive CD4(+) T cells: the first signal is transmitted through T-cell receptors (TCRs) providing the specificity of the immune response and initiating the earliest signals leading to T-cell activation, the second signal through costimulatory receptors promoting the survival and clonal expansion of the antigen-primed T cells, and the third signal through cytokine receptors directing the differentiation of naive CD4(+) T cells into the various T-H subsets. Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs), which are composed of six TRAF proteins (TRAF1-TRAF6) with a conserved C-terminal TRAF domain, are intracellular signaling adaptors that mediate the link between receptor-proximal activation events and intracellular signaling proteins. There is growing evidence that TRAFs recruited to TCRs, costimulatory TNFRs, and cytokine receptors play crucial roles in key signaling events in CD4(+) T cells and control the lineage commitment, functionality, and life-and-death decisions of different TH subsets. In this review, we summarize the TRAFs' physiological functions in T-cell immunity and the molecular mechanisms by which TRAFs regulate the three signals required for the activation, differentiation, and survival of CD4(+) T cells and other T-cell subsets.
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