{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T01:56:32Z","timestamp":1789955792606,"version":"4.0.1"},"reference-count":42,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2017,12,1]],"date-time":"2017-12-01T00:00:00Z","timestamp":1512086400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"JSPS","award":["JP25460512"],"award-info":[{"award-number":["JP25460512"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2017,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Interleukin17A (IL-17A) is known to be involved in the host defense against pathogens and the pathogenesis of autoimmune diseases. Previously, we showed that excessive amounts of interferon gamma (IFN-\u03b3) play an important role in the pathogenesis of the lethal effects of\n            <jats:named-content content-type=\"genus-species\">Toxoplasma gondii<\/jats:named-content>\n            by inducing anaphylactic responses. In the study described in this report, we examined the effects of IL-17A deficiency on murine host defense against oral\n            <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n            infection. IL-17A-deficient C57BL\/6 (B6) mice exhibited higher rates of mortality than wild-type (WT) mice during the acute phase of\n            <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n            infection. CD4\n            <jats:sup>+<\/jats:sup>\n            T cells in the mesenteric lymph nodes (mLNs) and ileum of\n            <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n            -infected IL-17A-deficient mice produced higher levels of IFN-\u03b3 than did those of WT mice. In addition, the level of\n            <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n            HSP70 (\n            <jats:italic>T.g<\/jats:italic>\n            .HSP70) expression was also significantly increased in the ileum, mLNs, liver, and spleen of infected IL-17A-deficient mice compared with that in WT mice. These elevated levels of expression of\n            <jats:italic>T.g<\/jats:italic>\n            .HSP70 and IFN-\u03b3 in infected IL-17A-deficient mice were presumably linked to the IL-17A defect since they decreased to WT levels after treatment with recombinant IL-17A. Furthermore, IL-17A-deficient mice were highly susceptible to the anaphylactic effect of\n            <jats:italic>T.g<\/jats:italic>\n            .HSP70, and the survival of IL-17A-deficient mice during the acute phase was improved by treatment with an anti-\n            <jats:italic>T.g<\/jats:italic>\n            .HSP70 monoclonal antibody. These results suggest that IL-17A plays an important role in host survival against\n            <jats:named-content content-type=\"genus-species\">T. gondii<\/jats:named-content>\n            infection by protecting the host from an anaphylactic reaction via the downregulation of\n            <jats:italic>T.g<\/jats:italic>\n            .HSP70 and IFN-\u03b3 production.\n          <\/jats:p>","DOI":"10.1128\/iai.00399-17","type":"journal-article","created":{"date-parts":[[2017,9,12]],"date-time":"2017-09-12T00:40:30Z","timestamp":1505176830000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":31,"title":["Interleukin-17A-Deficient Mice Are Highly Susceptible to Toxoplasma gondii Infection Due to Excessively Induced T. gondii HSP70 and Interferon Gamma Production"],"prefix":"10.1128","volume":"85","author":[{"given":"Masataka","family":"Moroda","sequence":"first","affiliation":[{"name":"Department of Infection and Host Defense, Graduate School of Medicine, Chiba University, Chiba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaya","family":"Takamoto","sequence":"additional","affiliation":[{"name":"Department of Infection and Host Defense, Graduate School of Medicine, Shinshu University, Matsumoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoichiro","family":"Iwakura","sequence":"additional","affiliation":[{"name":"Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Nakayama","sequence":"additional","affiliation":[{"name":"Department of Molecular Pathology, Graduate School of Medicine, Shinshu University, Matsumoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fumie","family":"Aosai","sequence":"additional","affiliation":[{"name":"Department of Infection and Host Defense, Graduate School of Medicine, Chiba University, Chiba, Japan"},{"name":"Department of Infection and Host Defense, Graduate School of Medicine, Shinshu University, Matsumoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","volume-title":"Toxoplasmosis of animals and humans","author":"Dubey JP","year":"2010","unstructured":"Dubey JP . 2010. 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