| First Author | Bruchard M | Year | 2015 |
| Journal | Nat Immunol | Volume | 16 |
| Issue | 8 | Pages | 859-70 |
| PubMed ID | 26098997 | Mgi Jnum | J:224866 |
| Mgi Id | MGI:5689221 | Doi | 10.1038/ni.3202 |
| Citation | Bruchard M, et al. (2015) The receptor NLRP3 is a transcriptional regulator of TH2 differentiation. Nat Immunol 16(8):859-70 |
| abstractText | The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1beta (IL-1beta) 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 (TH2) transcriptional program in a cell-intrinsic manner. NLRP3, but not the inflammasome adaptor ASC or caspase-1, positively regulated a TH2 program. In TH2 cells, NLRP3 bound the Il4 promoter and transactivated it in conjunction with the transcription factor IRF4. Nlrp3-deficient TH2 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 TH2 differentiation. |
