| First Author | Griffith JW | Year | 2023 |
| Journal | Nat Immunol | Volume | 24 |
| Issue | 12 | Pages | 2091-2107 |
| PubMed ID | 37945820 | Mgi Jnum | J:358215 |
| Mgi Id | MGI:7778487 | Doi | 10.1038/s41590-023-01655-2 |
| Citation | Griffith JW, et al. (2023) Regulatory T cell-derived IL-1Ra suppresses the innate response to respiratory viral infection. Nat Immunol 24(12):2091-2107 |
| abstractText | Regulatory T (T(reg)) cell modulation of adaptive immunity and tissue homeostasis is well described; however, less is known about T(reg) cell-mediated regulation of the innate immune response. Here we show that deletion of ST2, the receptor for interleukin (IL)-33, on T(reg) cells increased granulocyte influx into the lung and increased cytokine production by innate lymphoid and gammadelta T cells without alteration of adaptive immunity to influenza. IL-33 induced high levels of the interleukin-1 receptor antagonist (IL-1Ra) in ST2(+) T(reg) cells and deletion of IL-1Ra in T(reg) cells increased granulocyte influx into the lung. T(reg) cell-specific deletion of ST2 or IL-1Ra improved survival to influenza, which was dependent on IL-1. Adventitial fibroblasts in the lung expressed high levels of the IL-1 receptor and their chemokine production was suppressed by T(reg) cell-produced IL-1Ra. Thus, we define a new pathway where IL-33-induced IL-1Ra production by tissue T(reg) cells suppresses IL-1-mediated innate immune responses to respiratory viral infection. |
