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- W4313305880 abstract "Abstract Missense mutations in the Nod-like receptor Nlrp12 are associated with periodic fever syndromes and atopic dermatitis in humans, however the cellular and molecular mechanisms involved in NLRP12-mediated regulation of immune responses remain poorly defined. In this study, we focused on identifying the roles of NLRP12 in shaping inflammatory T cell responses and T cell-mediated disease. We found that immunization of NLRP12-deficient mice with myelin antigen to induce experimental autoimmune encephalomyelitis (EAE) provoked the generation of hyperinflammatory T cell responses in the periphery. Surprisingly, NLRP12-deficiency did not cause exacerbated forms of paralyzing EAE disease, instead Nlrp12-/- mice developed atypical neuroinflammatory symptoms that were characterized by ataxia and loss of balance. Non-classical EAE pathogenesis was characterized by altered regulation of canonical and non-canonical NF-kB signaling in the CNS. Furthermore, enhanced IL-4 production was identified to promote the development of atypical EAE disease in Nlrp12-/- mice. Interestingly, Nlrp12 was found to be highly expressed in T cells and purified NLRP12-deficient T cells exhibited hyperproliferation and enhanced NF-kB signaling in response to TCR stimulation. These results define an unexpected role for NLRP12 as an intrinsic negative regulator of T cell-mediated immunity, and identify altered NF-kB regulation and IL-4 production as key mediators of NLRP12-associated disease." @default.
- W4313305880 created "2023-01-06" @default.
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- W4313305880 date "2015-05-01" @default.
- W4313305880 modified "2023-09-26" @default.
- W4313305880 title "NLRP12 negatively regulates autoinflammatory disease by modulating T cell responses and IL-4 production (BA6P.133)" @default.
- W4313305880 doi "https://doi.org/10.4049/jimmunol.194.supp.114.14" @default.
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