{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T12:59:48Z","timestamp":1785416388026,"version":"3.56.0"},"reference-count":71,"publisher":"Life Science Alliance, LLC","issue":"9","license":[{"start":{"date-parts":[[2025,7,18]],"date-time":"2025-07-18T00:00:00Z","timestamp":1752796800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["life-science-alliance.org"],"crossmark-restriction":true},"short-container-title":["Life Sci. Alliance"],"accepted":{"date-parts":[[2025,6,25]]},"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:p>\n                    <jats:italic>Cryptosporidium parvum<\/jats:italic>\n                    infects intestinal epithelial cells, causing cryptosporidiosis in humans and neonatal livestock. Autophagy is an important component of the defense against\n                    <jats:italic>C. parvum<\/jats:italic>\n                    infection. IFITM3 is an IFN-stimulated gene that regulates viral infection through autophagy; however, its role in\n                    <jats:italic>C. parvum<\/jats:italic>\n                    infection is unknown. Herein, IFITM3 levels increased significantly after\n                    <jats:italic>C. parvum<\/jats:italic>\n                    infection and promoted autophagy.\n                    <jats:italic>IFITM3<\/jats:italic>\n                    overexpression up-regulated LC3B II\/LC3B I, Beclin-1, ATG7, and ATG5, but down-regulated p62 during infection. In\n                    <jats:italic>C. parvum<\/jats:italic>\n                    -infected HCT-8 cells, IFITM3 interacted with LC3B, Beclin-1, and ATG5.\n                    <jats:italic>IFITM3<\/jats:italic>\n                    knockdown or autophagy-inhibitor treatment decreased the ratio of LC3B II\/LC3B I, Beclin-1, ATG7, and ATG5, but increased p62 expression. Furthermore, IFITM3-regulated autophagy was associated with the inflammatory response, cell survival, and\n                    <jats:italic>C. parvum<\/jats:italic>\n                    clearance.\n                    <jats:italic>IFITM3<\/jats:italic>\n                    overexpression inhibited apoptosis, increased inflammatory cytokine IL-8 production, and decreased the cellular\n                    <jats:italic>C. parvum<\/jats:italic>\n                    burden.\n                    <jats:italic>IFITM3<\/jats:italic>\n                    silencing had the opposite effects. IFITM3 expression was positively regulated by STAT1 during infection, whereas\n                    <jats:italic>IFITM3<\/jats:italic>\n                    knockdown increased STAT1\u2019s compensatory effect. Thus, intestinal epithelial cells resist\n                    <jats:italic>C. parvum<\/jats:italic>\n                    infection via autophagy through the STAT1-IFITM3 axis.\n                  <\/jats:p>","DOI":"10.26508\/lsa.202503200","type":"journal-article","created":{"date-parts":[[2025,7,18]],"date-time":"2025-07-18T16:30:10Z","timestamp":1752856210000},"page":"e202503200","update-policy":"https:\/\/doi.org\/10.26508\/lsa.crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["STAT1-IFITM3 promotes autophagy in epithelial cells to control\n                    <i>Cryptosporidium parvum<\/i>\n                    infection"],"prefix":"10.26508","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2362-8864","authenticated-orcid":true,"given":"Lijun","family":"Cui","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03wneb138","id-type":"ROR","asserted-by":"publisher"}],"name":"National Key Laboratory of Intelligent Tracking and 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