Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 290, Issue 2, Pages 861-871Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M114.586560
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Funding
- 973 Project [2011CB910502]
- National Natural Science Foundation of China [30871286, 31071225, 31030040, 91229203]
- Tsinghua Science Foundation [20121080018]
- Natural Science Foundation of Beijing [511003]
- Major Program [2013ZX08011-006]
- 863 project in China [2012AA021703]
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TNF receptor 2 (TNFR2) exerts diverse roles in the pathogenesis of inflammatory and autoimmune diseases. Here, we report that TNFR2 but not TNFR1 forms a heteromer with interleukin-17 receptor D (IL-17RD), also named Sef, to activate NF-kappa B signaling. TNFR2 associates with IL-17RD, leading to mutual receptor aggregation and TRAF2 recruitment, which further activate the downstream cascade of NF-kappa B signaling. Depletion of IL-17RD impaired TNFR2-mediated activation of NF-kappa B signaling. Importantly, IL-17RD was markedly increased in renal tubular epithelial cells in nephritis rats, and a strong interaction of TNFR2 and IL-17RD was observed in the renal epithelia. The IL-17RD center dot TNFR2 complex in activation of NF-kappa B may explain the role of TNFR2 in inflammatory diseases including nephritis.
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