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Mice with mutations in the Crohn\u2019s disease susceptibility gene\n                  <jats:italic>Atg16l1<\/jats:italic>\n                  are susceptible to inflammation associated with intestinal epithelial cell (IEC) death, including loss of antimicrobial Paneth cells triggered by infection with murine norovirus (MNV). Here, we show that intestinal disease downstream of MNV depends on IFN-\u03b1\/\u03b2 and IFN-\u03bb signaling in IECs. In mouse organoids, IFNs synergize with TNF to induce RIPK1-dependent cell death, amplified by ATG16L1 deficiency. We further show that human intestinal organoids harboring the\n                  <jats:italic>ATG16L1<\/jats:italic>\n                  risk allele exhibit heightened sensitivity to TNF and IFN co-stimulation and to serum from severe COVID-19 patients. Our findings reveal that virally triggered cytokines including IFNs exacerbate epithelial vulnerability in genetically predisposed hosts.\n                <\/jats:p>","DOI":"10.64898\/2026.01.10.698817","type":"posted-content","created":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T00:40:11Z","timestamp":1768264811000},"source":"Crossref","is-referenced-by-count":1,"title":["Type I and III interferons synergize with TNF to promote virally-triggered damage to the intestinal epithelium"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8482-280X","authenticated-orcid":false,"given":"Lucie","family":"Bernard-Raichon","sequence":"first","affiliation":[{"name":"Kimmel Center for Biology and Medicine at the Skirball Institute, New York University Grossman School of Medicine, New York, NY, USA"},{"name":"Department of Microbiology, New York University Grossman School of Medicine, New York, NY, USA"},{"name":"Division of Gastroenterology and Hepatology, Department 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