{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T01:46:28Z","timestamp":1793151988301,"version":"4.5.0"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"American Gastroenterology Association and by the National Institute of Diabetes and Digestive and Kidney Diseases","award":["DK120320"],"award-info":[{"award-number":["DK120320"]}]},{"DOI":"10.13039\/100006975","name":"Indiana Clinical and Translational Sciences Institute","doi-asserted-by":"publisher","award":["UM1TR004402"],"award-info":[{"award-number":["UM1TR004402"]}],"id":[{"id":"10.13039\/100006975","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,5,14]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The cause of inflammatory bowel disease (IBD) is not known, but both innate and adaptive immunity contribute to IBD pathogenesis. To better understand the contributions of innate immunity to IBD, we have generated a mouse model of IBD that occurs spontaneously in the absence of adaptive immunity. This model is 100% penetrant, early onset, and driven by microbes. Here, we report that the colitis in this model exhibits extensive cell death in the gut mucosa, including cell death with features of apoptosis, necroptosis, and pyroptosis. This innate colitis and mucosal cell death was dependent on tumor necrosis factor (TNF). Deletion of interferon \u03b3 (IFN\u03b3) markedly suppressed cell death and release of interleukin 1 (IL1) in the intestinal mucosa but did not prevent colitis. Production of TNF by monocyte lineage cells was dependent on IFN\u03b3, but neutrophil production of TNF was independent of IFN\u03b3. Depletion of TNF in IFN\u03b3-deficient mice suppressed innate colitis. Thus, IFN\u03b3 is required for cell death and release of IL1 in the gut mucosa but is dispensable for innate colitis. These results indicate that TNF and IFN\u03b3 synergize to promote gut mucosal cell death but that TNF alone can drive innate colitis when cell death and IL1 release are reduced by the absence of IFN\u03b3.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag111","type":"journal-article","created":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T15:34:09Z","timestamp":1779377649000},"source":"Crossref","is-referenced-by-count":2,"title":["Synergism of TNF and IFN\u03b3 promotes cell death, but TNF drives innate immune-mediated colitis independent of IFN\u03b3"],"prefix":"10.1093","volume":"215","author":[{"given":"Alvaro","family":"Torres-Huerta","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Indiana University School of Medicine \u2013 South Bend , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katelyn","family":"Ruley-Haase","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Notre Dame , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonia","family":"Boger-May","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Indiana University School of Medicine \u2013 South Bend , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arpitha","family":"Mysore-Rajashekara","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Notre Dame , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theodore","family":"Reed","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Notre Dame , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morgan","family":"Hiller","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Notre Dame , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren","family":"Mayer","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Notre Dame , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madeleine","family":"Frech","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Notre Dame , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren","family":"Hollmer","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Notre Dame , South Bend, IN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Kolodychak","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Notre Dame , South Bend, IN,","place":["United 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