{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T20:07:49Z","timestamp":1789762069248,"version":"4.0.1"},"reference-count":63,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2018,4,1]],"date-time":"2018-04-01T00:00:00Z","timestamp":1522540800000},"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":[[2018,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>IL-27 is an immunoregulatory cytokine consisting of p28 and EBI3. Its receptor also has two subunits, WSX1 and gp130. Although IL-27 promotes Th1 differentiation in naive T cells, it also induces IL-10 expression in effector Th1 cells to curtail excessive immune responses. By using p28-deficient mice and WSX1-deficient mice (collectively called IL-27\u2013deficient mice), we examined the role of IL-27 in primary infection by murine \u03b3-herpesvirus 68 (MHV68), a murine model of EBV. Upon airway infection with MHV68, IL-27\u2013deficient mice had more aggravated lung inflammation than wild-type mice, although MHV68 infection per se was better controlled in IL-27\u2013deficient mice. Although epithelial cells and alveolar macrophages were primarily infected by MHV68, interstitial macrophages and dendritic cells were the major producers of IL-27. The lung inflammation of IL-27\u2013deficient mice was characterized by more IFN-\u03b3\u2013producing CD8+ T cells and fewer IL-10\u2013producing CD8+ T cells than that of wild-type mice. An infectious mononucleosis\u2013like disease was also aggravated in IL-27\u2013deficient mice, with prominent splenomegaly and severe hepatitis. Infiltration of IFN-\u03b3\u2013producing effector cells and upregulation of the CXCR3 ligand chemokines CXCL9, CXCL10, and CXCL11 were noted in the liver of MHV68-infected mice. Oral neomycin effectively ameliorated hepatitis, with decreased production of these chemokines in the liver, suggesting that the intestinal microbiota plays a role in liver inflammation through upregulation of these chemokines. Collectively, IL-27 is essential for the generation of IL-10\u2013producing effector cells in primary infection by MHV68. Our findings may also provide new insight into the mechanism of hepatitis associated with infectious mononucleosis.<\/jats:p>","DOI":"10.4049\/jimmunol.1700412","type":"journal-article","created":{"date-parts":[[2018,3,2]],"date-time":"2018-03-02T16:50:27Z","timestamp":1520009427000},"page":"2703-2713","source":"Crossref","is-referenced-by-count":8,"title":["Murine \u03b3-Herpesvirus 68 Induces Severe Lung Inflammation in IL-27\u2013Deficient Mice with Liver Dysfunction Preventable by Oral Neomycin"],"prefix":"10.1093","volume":"200","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7984-207X","authenticated-orcid":false,"given":"Kyosuke","family":"Kanai","sequence":"first","affiliation":[{"name":"Department of Microbiology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka 589-8511,","place":["Japan"]},{"name":"Division of Virology, Department of Microbiology and Immunology, Tottori University Faculty of Medicine , Yonago, Tottori 683-8503,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ah-Mee","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka 589-8511,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akiko","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka 589-8511,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomohiro","family":"Arikawa","sequence":"additional","affiliation":[{"name":"Division of General Education, Department of Biology, Kanazawa Medical University , Uchinada, Kahoku-gun, Ishikawa 920-0293,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teruhito","family":"Yasui","sequence":"additional","affiliation":[{"name":"Laboratory of Infectious Diseases and Immunity, National Institute of Biomedical Innovation, Health and Nutrition , Ibaraki, Osaka 567-0085,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroki","family":"Yoshida","sequence":"additional","affiliation":[{"name":"Division of Molecular and Cellular Immunoscience, Department of Biomolecular Sciences, Faculty of Medicine, Saga University , Saga 840-8502,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1798-714X","authenticated-orcid":false,"given":"Ikuo","family":"Tsunoda","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka 589-8511,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Osamu","family":"Yoshie","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka 589-8511,","place":["Japan"]},{"name":"The Health and Kampo Institute , Sendai, Miyagi 981-3205,","place":["Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2018,4,15]]},"reference":[{"key":"2025030610143007500_r1","doi-asserted-by":"crossref","first-page":"787","DOI":"10.1146\/annurev-immunol-032414-112326","article-title":"The immunology of Epstein-Barr virus-induced disease","volume":"33","author":"Taylor","year":"2015","journal-title":"Annu. 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