{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T01:21:19Z","timestamp":1792113679598,"version":"4.4.0"},"reference-count":46,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2013,8,19]],"date-time":"2013-08-19T00:00:00Z","timestamp":1376870400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"KAKENHI","award":["24117504"],"award-info":[{"award-number":["24117504"]}]},{"name":"KAKENHI","award":["25650226"],"award-info":[{"award-number":["25650226"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2013,10]]},"abstract":"Although IL<\/jats:styled-content>\u201012 is believed to contribute to protective immune responses, the role played by IL<\/jats:styled-content>\u201023 (a member of the IL<\/jats:styled-content>\u201012 family) in malaria is elusive. Here, we show that IL<\/jats:styled-content>\u201023 is produced during infection with Plasmodium berghei<\/jats:italic> NK<\/jats:styled-content>65. Mice deficient in IL<\/jats:styled-content>\u201023 (p19KO<\/jats:styled-content>) had higher parasitemia and died earlier than wild\u2010type (WT<\/jats:styled-content>) controls. Interestingly, p19KO<\/jats:styled-content> mice had lower numbers of IL<\/jats:styled-content>\u201017\u2010producing splenic cells than their WT<\/jats:styled-content> counterparts. Furthermore, mice deficient in IL<\/jats:styled-content>\u201017 (17KO<\/jats:styled-content>) suffered higher parasitemia than the WT<\/jats:styled-content> controls, indicating that IL<\/jats:styled-content>\u201023\u2010mediated protection is dependent on induction of IL<\/jats:styled-content>\u201017 during infection. We found that macrophages were responsible for IL<\/jats:styled-content>\u201017 production in response to IL<\/jats:styled-content>\u201023. We observed a striking reduction in splenic macrophages in the p19KO<\/jats:styled-content> and 17KO<\/jats:styled-content> mice, both of which became highly susceptible to infection. Thus, IL<\/jats:styled-content>\u201017 appears to be crucial for maintenance of splenic macrophages. Adoptive transfer of macrophages into macrophage\u2010depleted mice confirmed that macrophage\u2010derived IL<\/jats:styled-content>\u201017 is required for macrophage accumulation and parasite eradication in the recipient mice. We also found that IL<\/jats:styled-content>\u201017 induces CCL<\/jats:styled-content>2\/7, which recruit macrophages. Our findings reveal a novel protective mechanism whereby IL<\/jats:styled-content>\u201023, IL<\/jats:styled-content>\u201017, and macrophages reduce the severity of infection with blood\u2010stage malaria parasites.<\/jats:p>","DOI":"10.1002\/eji.201343493","type":"journal-article","created":{"date-parts":[[2013,7,10]],"date-time":"2013-07-10T12:14:41Z","timestamp":1373458481000},"page":"2696-2706","source":"Crossref","is-referenced-by-count":30,"title":["IL<\/scp>\u201023 protection against P<\/scp>lasmodium berghei<\/i> infection in mice is partially dependent on IL<\/scp>\u201017 from macrophages"],"prefix":"10.1002","volume":"43","author":[{"given":"Hidekazu","family":"Ishida","sequence":"first","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takashi","family":"Imai","sequence":"additional","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazutomo","family":"Suzue","sequence":"additional","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Makoto","family":"Hirai","sequence":"additional","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomoyo","family":"Taniguchi","sequence":"additional","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akihiko","family":"Yoshimura","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology School of Medicine Keio University Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoichiro","family":"Iwakura","sequence":"additional","affiliation":[{"name":"Center for Experimental Medicine Institute of Medical Science The University of Tokyo Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroko","family":"Okada","sequence":"additional","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomohisa","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chikako","family":"Shimokawa","sequence":"additional","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hajime","family":"Hisaeda","sequence":"additional","affiliation":[{"name":"Department of Parasitology Graduate School of Medicine Gunma University Maebashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,8,19]]},"reference":[{"key":"e_1_2_7_2_1","unstructured":"WHO.Malaria Fact sheet No. 94 2013. 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