{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T13:11:12Z","timestamp":1790169072594,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2017,2,1]],"date-time":"2017-02-01T00:00:00Z","timestamp":1485907200000},"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":[[2017,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Early-life wheezing-associated infections with rhinovirus (RV) have been associated with asthma development in children. We have shown that RV infection of 6-day-old mice induces mucous metaplasia and airways hyperresponsiveness, which is dependent on IL-13, IL-25, and type 2 innate lymphoid cells (ILC2s). Infection of immature mice fails to induce lung IFN-\u03b3 expression, in contrast to mature 8-week-old mice with a robust IFN-\u03b3 response, consistent with the notion that deficient IFN-\u03b3 production in immature mice permits RV-induced type 2 immune responses. We therefore examined the effects of intranasal IFN-\u03b3 administration on RV-induced ILC2 expansion and IL-13 expression in 6-day-old BALB\/c and IL-13 reporter mice. Airway responses were assessed by histology, immunofluorescence microscopy, quantitative polymerase chain reaction, ELISA, and flow cytometry. Lung ILC2s were also treated with IFN-\u03b3 ex vivo. We found that, compared with untreated RV-infected immature mice, IFN-\u03b3 treatment attenuated RV-induced IL-13 and Muc5ac mRNA expression and mucous metaplasia. IFN-\u03b3 also reduced ILC2 expansion and the percentage of IL-13\u2013secreting ILC2s. IFN-\u03b3 had no effect on the mRNA or protein expression of IL-25, IL-33, or thymic stromal lymphoprotein. Finally, IFN-\u03b3 treatment of sorted ILC2s reduced IL-5, IL-13, IL-17RB, ST2, and GATA-3 mRNA expression. We conclude that, in immature mice, IFN-\u03b3 inhibits ILC2 expansion and IL-13 expression in vivo and ex vivo, thereby attenuating RV-induced mucous metaplasia. These findings demonstrate the antagonistic function of IFN-\u03b3 on ILC2 expansion and gene expression, the absence of which may contribute to the development of an asthma-like phenotype after early-life RV infection.<\/jats:p>","DOI":"10.1165\/rcmb.2016-0056oc","type":"journal-article","created":{"date-parts":[[2016,9,28]],"date-time":"2016-09-28T16:54:25Z","timestamp":1475081665000},"page":"242-251","source":"Crossref","is-referenced-by-count":59,"title":["IFN-\u03b3 Blocks Development of an Asthma Phenotype in Rhinovirus-Infected Baby Mice by Inhibiting Type 2 Innate Lymphoid Cells"],"prefix":"10.1093","volume":"56","author":[{"given":"Mingyuan","family":"Han","sequence":"first","affiliation":[{"name":"Departments of Pediatrics and Communicable Diseases, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun Young","family":"Hong","sequence":"additional","affiliation":[{"name":"Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suraj","family":"Jaipalli","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Communicable Diseases, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charu","family":"Rajput","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Communicable Diseases, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Lei","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Communicable Diseases, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanna L.","family":"Hinde","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Communicable Diseases, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Chen","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Communicable Diseases, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalie M.","family":"Hershenson","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics and Communicable Diseases, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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