{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T04:57:40Z","timestamp":1791262660398,"version":"4.1.0"},"reference-count":41,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2012,3,1]],"date-time":"2012-03-01T00:00:00Z","timestamp":1330560000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The roles of Th1 and Th17 responses as mediators of host protection and pathology in the intestine are the subjects of intense research. In this study, we investigated a model of intestinal inflammation driven by the intracellular apicomplexan parasite Eimeria falciformis. Although IFN-\u03b3 was the predominant cytokine during E. falciformis infection in wild-type mice, it was found to be dispensable for host defense and the development of intestinal inflammation. E. falciformis-infected IFN-\u03b3R\u2212\/\u2212 and IFN-\u03b3\u2212\/\u2212 mice developed dramatically exacerbated body weight loss and intestinal pathology, but they surprisingly harbored fewer parasites. This was associated with a striking increase in parasite-specific IL-17A and IL-22 production in the mesenteric lymph nodes and intestine. CD4+ T cells were found to be the source of IL-17A and IL-22, which drove the recruitment of neutrophils and increased tissue expression of anti-microbial peptides (RegIII\u03b2, RegIII\u03b3) and matrix metalloproteinase 9. Concurrent neutralization of IL-17A and IL-22 in E. falciformis-infected IFN-\u03b3R\u2212\/\u2212 mice resulted in a reduction in infection-induced body weight loss and inflammation and significantly increased parasite shedding. In contrast, neutralization of IL-22 alone was sufficient to increase parasite burden, but it had no effect on body weight loss. Treatment of an E. falciformis-infected intestinal epithelial cell line with IFN-\u03b3, IL-17A, or IL-22 significantly reduced parasite development in vitro. Taken together, to our knowledge these data demonstrate for the first time an antiparasite effect of IL-22 during an intestinal infection, and they suggest that IL-17A and IL-22 have redundant roles in driving intestinal pathology in the absence of IFN-\u03b3 signaling.<\/jats:p>","DOI":"10.4049\/jimmunol.1102062","type":"journal-article","created":{"date-parts":[[2012,1,21]],"date-time":"2012-01-21T07:51:34Z","timestamp":1327132294000},"page":"2410-2418","source":"Crossref","is-referenced-by-count":49,"title":["IL-22 Mediates Host Defense against an Intestinal Intracellular Parasite in the Absence of IFN-\u03b3 at the Cost of Th17-Driven Immunopathology"],"prefix":"10.1093","volume":"188","author":[{"given":"J\u00f6rg","family":"Stange","sequence":"first","affiliation":[{"name":"Molekulare Parasitologie, Humboldt Universit\u00e4t zu Berlin , D-10115 Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew R","family":"Hepworth","sequence":"additional","affiliation":[{"name":"Molekulare Parasitologie, Humboldt Universit\u00e4t zu Berlin , D-10115 Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sebastian","family":"Rausch","sequence":"additional","affiliation":[{"name":"Molekulare Parasitologie, Humboldt Universit\u00e4t zu Berlin , D-10115 Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lara","family":"Zajic","sequence":"additional","affiliation":[{"name":"Molekulare Parasitologie, Humboldt Universit\u00e4t zu Berlin , D-10115 Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anja A","family":"K\u00fchl","sequence":"additional","affiliation":[{"name":"Institute of Pathology\/Research Center ImmunoSciences, Charit\u00e9\u2013Campus Benjamin Franklin , 12203 Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine","family":"Uyttenhove","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research , B-1200 Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Christophe","family":"Renauld","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research , B-1200 Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susanne","family":"Hartmann","sequence":"additional","affiliation":[{"name":"Molekulare Parasitologie, Humboldt Universit\u00e4t zu Berlin , D-10115 Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Lucius","sequence":"additional","affiliation":[{"name":"Molekulare Parasitologie, Humboldt Universit\u00e4t zu Berlin , D-10115 Berlin ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,3,1]]},"reference":[{"key":"2025032409565858700_r1","doi-asserted-by":"crossref","first-page":"1742","DOI":"10.1126\/science.8456301","article-title":"Immune response in mice that lack the interferon-\u03b3 receptor","volume":"259","author":"Huang","year":"1993","journal-title":"Science"},{"key":"2025032409565858700_r2","doi-asserted-by":"crossref","first-page":"218","DOI":"10.1016\/j.micinf.2009.12.005","article-title":"CD8+ cells protect mice against reinfection with the intestinal parasite Eimeria falciformis","volume":"12","author":"Pogonka","year":"2010","journal-title":"Microbes Infect."},{"key":"2025032409565858700_r3","doi-asserted-by":"crossref","first-page":"1083","DOI":"10.1084\/jem.189.7.1083","article-title":"Effector cells of both nonhemopoietic and hemopoietic origin are required for interferon (IFN)-\u03b3- and tumor necrosis factor (TNF)-\u03b1-dependent host resistance to the intracellular pathogen, Toxoplasma gondii","volume":"189","author":"Yap","year":"1999","journal-title":"J. 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