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T cell-intrinsic ASC critically promotes T(H)17-mediated experimental autoimmune encephalomyelitis

Author:
Martin, Bradley N.  Wang, Chenhui  Zhang, Cun-jin  Kang, Zizhen  Gulen, Muhammet Fatih  Zepp, Jarod A.  Zhao, Junjie  Bian, Guanglin  Do, Jeong-su  Min, Booki  Pavicic, Paul G., Jr.  El-Sanadi, Caroline  Fox, Paul L.  Akitsu, Aoi  Iwakura, Yoichiro  Sarkar, Anasuya  Wewers, Mark D.  Kaiser, William J.  Mocarski, Edward S.  Rothenberg, Marc E.  Hise, Amy G.  Dubyak, George R.  Ransohoff, Richard M.  Li, Xiaoxia  


Journal:
NATURE IMMUNOLOGY


Issue Date:
2016


Abstract(summary):

Interleukin 1 beta (IL-1 beta) is critical for the in vivo survival, expansion and effector function of IL-17-producing helper T (T(H)17) cells during autoimmune responses, including experimental autoimmune encephalomyelitis (EAE). However, the spatiotemporal role and cellular source of IL-1 beta during EAE pathogenesis are poorly defined. In the present study, we uncovered a T cell-intrinsic inflammasome that drives IL-1 beta production during T(H)17-mediated EAE pathogenesis. Activation of T cell antigen receptors induced expression of pro-IL-1 beta, whereas ATP stimulation triggered T cell production of IL-1 beta via ASC-NLRP3-dependent caspase-8 activation. IL-1R was detected on T(H)17 cells but not on type 1 helper T (T(H)1) cells, and ATP-treated T(H)17 cells showed enhanced survival compared with ATP-treated T(H)1 cells, suggesting autocrine action of T(H)17-derived IL-1 beta. Together these data reveal a critical role for IL-1 beta produced by a T(H)17 cell-intrinsic ASC-NLRP3-caspase-8 inflammasome during inflammation of the central nervous system.


Page:
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