| First Author | Gullicksrud JA | Year | 2022 |
| Journal | Mucosal Immunol | Volume | 15 |
| Issue | 2 | Pages | 362-372 |
| PubMed ID | 34750455 | Mgi Jnum | J:360458 |
| Mgi Id | MGI:7797586 | Doi | 10.1038/s41385-021-00468-6 |
| Citation | Gullicksrud JA, et al. (2022) Enterocyte-innate lymphoid cell crosstalk drives early IFN-gamma-mediated control of Cryptosporidium. Mucosal Immunol 15(2):362-372 |
| abstractText | The intestinal parasite, Cryptosporidium, is a major contributor to global child mortality and causes opportunistic infection in immune deficient individuals. Innate resistance to Cryptosporidium, which specifically invades enterocytes, is dependent on the production of IFN-gamma, yet whether enterocytes contribute to parasite control is poorly understood. In this study, utilizing a mouse-adapted strain of C. parvum, we show that epithelial-derived IL-18 synergized with IL-12 to stimulate innate lymphoid cell (ILC) production of IFN-gamma required for early parasite control. The loss of IFN-gamma-mediated STAT1 signaling in enterocytes, but not dendritic cells or macrophages, antagonized early parasite control. Transcriptional profiling of enterocytes from infected mice identified an IFN-gamma signature and enrichment of the anti-microbial effectors IDO, GBP, and IRG. Deletion experiments identified a role for Irgm1/m3 in parasite control. Thus, enterocytes promote ILC production of IFN-gamma that acts on enterocytes to restrict the growth of Cryptosporidium. |
