{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T13:36:28Z","timestamp":1791207388608,"version":"4.1.0"},"reference-count":36,"publisher":"The Company of Biologists","license":[{"start":{"date-parts":[[2021,5,18]],"date-time":"2021-05-18T00:00:00Z","timestamp":1621296000000},"content-version":"am","delay-in-days":2329,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,1,1]]},"abstract":"<jats:p>Acute schistosomiasis is featured by pro-inflammatory responses against tissue or organ trapped parasite ova along with granuloma formation. Herein in the present report we conducted studies in Cx3cr1-\/- mice and demonstrated the role of Cx3cr1 in the pathoetiology of granuloma formation during acute schistosomiasis. Mice deficient in Cx3cr1 were protected from S. japonicum egg-induced granuloma formation and hepatic injury as manifested by reduced body weight loss, attenuated hepatomegaly along with preserved liver function. Notably, S. japonicum infection induced high levels of hepatic Cx3cr1 expression, which was predominantly expressed by infiltrating macrophages. Loss of Cx3cr1 rendered macrophages preferentially toward M2 polarization, which then led to a characteristic switch of host immune defense in the setting of acute schistosomiasis from a conventional Th1 to typical Th2 response. This immune switch caused by Cx3cr1 deficiency was likely associated with enhanced STAT6\/PPAR-\u03b3 signaling and increased IDO expression. Together, our data provided feasible evidence supporting that CX3CR1 could be a viable therapeutic target for treatment of acute schistosomiasis.<\/jats:p>","DOI":"10.1242\/dmm.018242","type":"journal-article","created":{"date-parts":[[2015,4,22]],"date-time":"2015-04-22T01:52:16Z","timestamp":1429667536000},"source":"Crossref","is-referenced-by-count":22,"title":["<i>Cx3cr1<\/i>deficiency attenuates hepatic granuloma formation during acute schistosomiasis by enhancing M2-type polarization of macrophages"],"prefix":"10.1242","author":[{"given":"Lin","family":"Ran","sequence":"first","affiliation":[{"name":"Department of Molecular Biology, Medical College of Yangtze University, 1 Nanhuan Road, Jingzhou, Hubei, 434023, China"},{"name":"The Center for Biomedical Research, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, 430030, 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