| First Author | Brasseit J | Year | 2018 |
| Journal | Front Immunol | Volume | 9 |
| Pages | 23 | PubMed ID | 29416538 |
| Mgi Jnum | J:278222 | Mgi Id | MGI:6296220 |
| Doi | 10.3389/fimmu.2018.00023 | Citation | Brasseit J, et al. (2018) Divergent Roles of Interferon-gamma and Innate Lymphoid Cells in Innate and Adaptive Immune Cell-Mediated Intestinal Inflammation. Front Immunol 9:23 |
| abstractText | Aberrant interferon gamma (IFNgamma) expression is associated with the pathogenesis of numerous autoimmune- and inflammatory disorders, including inflammatory bowel diseases (IBD). However, the requirement of IFNgamma for the pathogenesis of chronic intestinal inflammation remains controversial. The aim of this study was thus to investigate the role of IFNgamma in experimental mouse models of innate and adaptive immune cell-mediated intestinal inflammation using genetically and microbiota-stabilized hosts. While we find that IFNgamma drives acute intestinal inflammation in the anti-CD40 colitis model in an innate lymphoid cell (ILC)-dependent manner, IFNgamma secreted by both transferred CD4 T cells and/or cells of the lymphopenic Rag1(-/-) recipient mice was dispensable for CD4 T cell-mediated colitis. In the absence of IFNgamma, intestinal inflammation in CD4 T cell recipient mice was associated with enhanced IL17 responses; consequently, targeting IL17 signaling in IFNgamma-deficient mice reduced T cell-mediated colitis. Intriguingly, in contrast to the anti-CD40 model of colitis, depletion of ILC in the Rag1(-/-) recipients of colitogenic CD4 T cells did not prevent induction of colonic inflammation. Together, our findings demonstrate that IFNgamma represents an essential, or a redundant, pro-inflammatory cytokine for the induction of intestinal inflammation, depending on the experimental mouse model used and on the nature of the critical disease inducing immune cell populations involved. |
