| First Author | Muñoz M | Year | 2015 |
| Journal | Immunity | Volume | 42 |
| Issue | 2 | Pages | 321-331 |
| PubMed ID | 25680273 | Mgi Jnum | J:223829 |
| Mgi Id | MGI:5660453 | Doi | 10.1016/j.immuni.2015.01.011 |
| Citation | Munoz M, et al. (2015) Interleukin-22 induces interleukin-18 expression from epithelial cells during intestinal infection. Immunity 42(2):321-31 |
| abstractText | T helper 1 (Th1) cell-associated immunity exacerbates ileitis induced by oral Toxoplasma gondii infection. We show here that attenuated ileitis observed in interleukin-22 (IL-22)-deficient mice was associated with reduced production of Th1-cell-promoting IL-18. IL-22 not only augmented the expression of Il18 mRNA and inactive precursor protein (proIL-18) in intestinal epithelial cells after T. gondii or Citrobacter rodentium infection, but also maintained the homeostatic amount of proIL-18 in the ileum. IL-22, however, did not induce the processing to active IL-18, suggesting a two-step regulation of IL-18 in these cells. Although IL-18 exerted pathogenic functions during ileitis triggered by T. gondii, it was required for host defense against C. rodentium. Conversely, IL-18 was required for the expression of IL-22 in innate lymphoid cells (ILCs) upon T. gondii infection. Our results define IL-18 as an IL-22 target gene in epithelial cells and describe a complex mutual regulation of both cytokines during intestinal infection. |
