期刊
NATURE IMMUNOLOGY
卷 16, 期 8, 页码 859-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3202
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资金
- French National Research Agency (Investissements d'Avenir program) [ANR-11-LABX-0021]
- Ligue nationale contre le cancer
- Fondation de France
- Institut National du Cancer
- Fondation ARC
- Conseil Regional de Bourgogne/INSERM
- French National Research Agency [ANR-13-JSV3-0001]
- Fondation pour l'aide a la Recherche sur la Sclerose en Plaques
- Ligue Regionale contre le cancer Comite Grand-Est
- European Commission [PCIG10-GA-2011-303719]
- Centre National de la Recherche Scientifique
- Fonds Europeen de Developpement Economique et Regional
- Le Stadium
- Orleans and Fondation pour la Recherche Medicale
- Agence Nationale de la Recherche (ANR) [ANR-13-JSV3-0001] Funding Source: Agence Nationale de la Recherche (ANR)
The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1 beta (IL-1 beta) and IL-18. Whether NLRP3 can shape immunological function independently of inflammasomes is unclear. We found that NLRP3 expression in CD4(+) T cells specifically supported a T helper type 2 (T(H)2) transcriptional program in a cell-intrinsic manner. NLRP3, but not the inflammasome adaptor ASC or caspase-1, positively regulated a T(H)2 program. In T(H)2 cells, NLRP3 bound the Il4 promoter and transactivated it in conjunction with the transcription factor IRF4. Nlrp3-deficient T(H)2 cells supported melanoma tumor growth in an IL-4-dependent manner and also promoted asthma-like symptoms. Our results demonstrate the ability of NLRP3 to act as a key transcription factor in T(H)2 differentiation.
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