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10.1016/j.immuni.2015.03.006

http://scihub22266oqcxt.onion/10.1016/j.immuni.2015.03.006
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suck abstract from ncbi


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pmid25888258      Immunity 2015 ; 42 (4): 654-64
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  • NLRP12 negatively regulates autoinflammatory disease by modulating interleukin-4 production in T cells #MMPMID25888258
  • Lukens JR; Gurung P; Shaw PJ; Barr MJ; Zaki MH; Brown S; Vogel P; Chi H; Kanneganti TD
  • Immunity 2015[Apr]; 42 (4): 654-64 PMID25888258show ga
  • Missense mutations in the nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain containing family of gene 12 (Nlrp12) are associated with periodic fever syndromes and atopic dermatitis in humans. Here, we have demonstrated a crucial role for NLRP12 in negatively regulating pathogenic T cell responses. Nlrp12?/? mice responded to antigen immunization with hyperinflammatory T cell responses. Furthermore, transfer of CD4+CD45RBhiNlrp12?/? T cells into immunodeficient mice led to more severe colitis and atopic dermatitis. NLRP12-deficiency did not, however, cause exacerbated ascending paralysis during experimental autoimmune encephalomyelitis (EAE), instead Nlrp12?/? mice developed atypical neuroinflammatory symptoms that were characterized by ataxia and loss of balance. Enhanced T cell-mediated interleukin-4 (IL-4) production promotes the development of atypical EAE disease in Nlrp12?/? mice. These results define an unexpected role for NLRP12 as an intrinsic negative regulator of T cell-mediated immunity, and identify altered NF-?B regulation and IL-4 production as key mediators of NLRP12-associated disease.



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