Tumor necrosis factor receptor (TNFR) associated factor 5 is a critical intermediate of costimulatory signaling pathways triggered by glucocorticoid-induced TNFR in T cells

doi:10.1074/jbc.M512915200

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Papers In Press, published online ahead of print February 1, 2006
J. Biol. Chem, 10.1074/jbc.M512915200
Submitted on December 2, 2005
Revised on January 31, 2006
Accepted on January 31, 2006

Tumor necrosis factor receptor (TNFR) associated factor 5 is a critical intermediate of costimulatory signaling pathways triggered by glucocorticoid-induced TNFR in T cells

Edward M. Esparza, Tullia Lindsten, Julia M. Stockhausen, and Robert H. Arch

Medicine, Washington University, School of Medicine, Saint Louis, MO 63110

Corresponding Author: arch{at}wustl.edu

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 (Treg cells) and co-stimulating T effector cells (Teff 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 (NF- $kappa$ B) as well as the mitogen-activated protein kinases (MAPKs) p38 and extracellular signal-regulated protein kinase (ERK), while activation of c-Jun N-terminal kinase (JNK) 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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