{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T06:04:29Z","timestamp":1791180269309,"version":"4.1.0"},"reference-count":63,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2004,12,3]],"date-time":"2004-12-03T00:00:00Z","timestamp":1102032000000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Scand J Immunol"],"published-print":{"date-parts":[[2004,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Sj\u00f6gren's syndrome\u2010like autoimmune exocrinopathy (AEC) in the nonobese diabetic (NOD) mouse progresses from a preimmune phase to an immune phase, resulting in dry mouth and\/or dry eyes. In the present study, the impact of the prototypical T\u2010helper type 1 cytokine, interferon\u2010gamma (IFN\u2010\u03b3), on the onset of AEC was investigated using both the IFN\u2010\u03b3 and the IFN\u2010\u03b3 receptor gene knockout mice, NOD.\n                    <jats:italic>IFN\u2010\u03b3<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    and NOD.\n                    <jats:italic>IFN\u2010\u03b3R<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    , respectively. Neither the NOD.\n                    <jats:italic>IFN\u2010\u03b3<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    nor the NOD.\n                    <jats:italic>IFN\u2010\u03b3R<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    mice exhibited increased acinar cell apoptosis and abnormal salivary protein expression, typically observed in parental NOD mice prior to disease. Without these preimmune phase abnormalities, NOD.\n                    <jats:italic>IFN\u2010\u03b3<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    and NOD.\n                    <jats:italic>IFN\u2010\u03b3R<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    mice showed no subsequent autoimmune responses against the salivary glands at 20 weeks. Interestingly, real\u2010time polymerase chain reaction and electrophoretic gel mobility shift assays suggested that IFN\u2010\u03b3 and STAT1, as well as the transcriptional activity of STAT1 in NOD glands, were increased at birth. Unlike the neonatal submandibular glands of NOD or NOD\u2010\n                    <jats:italic>scid<\/jats:italic>\n                    mice that show abnormal glandular morphogenesis at birth, the submandibular glands of the newly constructed congenic strain, NOD\u2010\n                    <jats:italic>scid<\/jats:italic>\n                    .\n                    <jats:italic>IFN\u2010\u03b3<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2013\/\u2013<\/jats:italic>\n                    <\/jats:sup>\n                    , were found to be normal. Taken together, IFN\u2010\u03b3 appears to play a critical role not only during the later immune phase of AEC, but also the early preimmune phase, independent of effector functions of immune cells. How exactly IFN\u2010\u03b3 functions during this period remains speculative.\n                  <\/jats:p>","DOI":"10.1111\/j.0300-9475.2004.01508.x","type":"journal-article","created":{"date-parts":[[2004,12,3]],"date-time":"2004-12-03T08:07:59Z","timestamp":1102061279000},"page":"552-565","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":139,"title":["A Dual Role for Interferon\u2010\u03b3 in the Pathogenesis of Sj\u00f6gren's Syndrome\u2010Like Autoimmune Exocrinopathy in the Nonobese Diabetic Mouse"],"prefix":"10.1111","volume":"60","author":[{"given":"S.","family":"Cha","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Brayer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Gao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V.","family":"Brown","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Killedar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"U.","family":"Yasunari","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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