| First Author | Zindl CL | Year | 2022 |
| Journal | Immunity | Volume | 55 |
| Issue | 3 | Pages | 494-511.e11 |
| PubMed ID | 35263568 | Mgi Jnum | J:324836 |
| Mgi Id | MGI:7281907 | Doi | 10.1016/j.immuni.2022.02.003 |
| Citation | Zindl CL, et al. (2022) A nonredundant role for T cell-derived interleukin 22 in antibacterial defense of colonic crypts. Immunity 55(3):494-511.e11 |
| abstractText | Interleukin (IL)-22 is central to immune defense at barrier sites. We examined the contributions of innate lymphoid cell (ILC) and T cell-derived IL-22 during Citrobacter rodentium (C.r) infection using mice that both report Il22 expression and allow lineage-specific deletion. ILC-derived IL-22 activated STAT3 in C.r-colonized surface intestinal epithelial cells (IECs) but only temporally restrained bacterial growth. T cell-derived IL-22 induced a more robust and extensive activation of STAT3 in IECs, including IECs lining colonic crypts, and T cell-specific deficiency of IL-22 led to pathogen invasion of the crypts and increased mortality. This reflected a requirement for T cell-derived IL-22 for the expression of a host-protective transcriptomic program that included AMPs, neutrophil-recruiting chemokines, and mucin-related molecules, and it restricted IFNgamma-induced proinflammatory genes. Our findings demonstrate spatiotemporal differences in the production and action of IL-22 by ILCs and T cells during infection and reveal an indispensable role for IL-22-producing T cells in the protection of the intestinal crypts. |
