Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 281, Issue 13, Pages 8559-8564Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M512915200
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- NHLBI NIH HHS [5 RO1 HL67312-02, T32 HL007317] Funding Source: Medline
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Tumor necrosis factor receptor ( TNFR) family members such as glucocorticoid-induced TNFR ( GITR) control T cell activation, differentiation, and effector functions. Importantly, GITR functions as a pivotal regulator of physiologic and pathologic immune responses by abrogating the suppressive effects of T regulatory cells and costimulating T effector cells. However, the molecular mechanisms underlying GITR-triggered signal transduction pathways remain unclear. Interestingly, GITR-induced stimulation of TNFR-associated factor ( TRAF) 5-deficient T cells resulted in decreased activation of nuclear factor kappa B as well as the mitogen-activated protein kinases p38 and extracellular signal-regulated protein kinase, whereas activation of c-Jun N-terminal kinase was less affected. Consistent with impaired signaling, costimulatory effects of GITR were diminished in TRAF5(-/-) T cells. In sum, our studies indicate that TRAF5 plays a crucial role in GITR-induced signaling pathways that augment T cell activation.
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