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The lack of IFN-\u03b3 responsiveness alters IFN-\u03b3-induced Ig class switching by B cells from these mice.<jats:italic>In vitro<\/jats:italic>cultures of T cells demonstrate that the T cells from the IFN-\u03b3R2 \u2212\/\u2212 mice have a defect in Th1 cell differentiation. The IFN-\u03b3R2 (\u2212\/\u2212) mice also produce lower amounts of IFN-\u03b3 in response to antigenic challenge. In addition, IFN-\u03b3R2 \u2212\/\u2212 mice are defective in contact hypersensitivity and are highly susceptible to infection by<jats:italic>Listeria monocytogenes<\/jats:italic>. These results demonstrate that the IFN-\u03b3R2 is essential for IFN-\u03b3-mediated immune responses<jats:italic>in vivo<\/jats:italic>.<\/jats:p>","DOI":"10.1073\/pnas.95.14.8233","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T14:39:15Z","timestamp":1027694355000},"page":"8233-8238","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":82,"title":["Targeted disruption of the interferon-\u03b3 receptor 2 gene results in severe immune defects in mice"],"prefix":"10.1073","volume":"95","author":[{"given":"Binfeng","family":"Lu","sequence":"first","affiliation":[{"name":"Integrated Program of Molecular, Cellular, and Biophysical Studies, and Departments of Microbiology and Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032; Preclinical Research, F. 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