{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T14:33:51Z","timestamp":1787063631835,"version":"build-2736575974"},"reference-count":29,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2013,3,26]],"date-time":"2013-03-26T00:00:00Z","timestamp":1364256000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Dent Res"],"published-print":{"date-parts":[[2013,5]]},"abstract":"<jats:p>\n                    In Sj\u00f6gren\u2019s Syndrome (SS), inherent glandular defects, autoimmunity, and mononuclear cell infiltration within the salivary glands cause reduced salivation leading to xerostomia. Excessive production of type I interferons (IFN), triggered by environmental and genetic factors, is considered pathogenic in this disorder. However, whether type I IFN production is causative or an outcome of the disease process is not known. To address this question, we introduced a deficiency of interferon alpha receptor 1 ( Ifnar1) into B6. Aec1Aec2 mice, which are known to have the genetic loci necessary for developing a SS-like disorder. This new mouse strain, B6. Aec1Aec2Ifnar1\n                    <jats:sup>-\/-<\/jats:sup>\n                    , lacking type I IFN-mediated signaling, was characterized for pilocarpine-induced salivation, the presence of serum autoantibodies, sialoadenitis, and dacryoadenitis. Compared with the B6. Aec1Aec2Ifnar1\n                    <jats:sup>+\/+<\/jats:sup>\n                    (wild-type) mice, the B6. Aec1Aec2Ifnar1\n                    <jats:sup>-\/-<\/jats:sup>\n                    (knockout) mice had significantly lower mononuclear cell infiltration in the salivary and lacrimal glands. The knockout mice were completely protected from salivary gland dysfunction. Surprisingly, they had a robust autoantibody response comparable with that of the wild-type mice. These findings demonstrate that, in the absence of type I IFN-mediated signaling, systemic autoantibody responses can be dissociated from glandular pathology. Our study suggests that, in genetically susceptible individuals, the type I IFN pathway can instigate certain features of SS.\n                  <\/jats:p>","DOI":"10.1177\/0022034513483315","type":"journal-article","created":{"date-parts":[[2013,3,27]],"date-time":"2013-03-27T01:10:17Z","timestamp":1364346617000},"page":"444-449","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":40,"title":["Type I Interferon Receptor Deficiency Prevents Murine Sj\u00f6gren\u2019s Syndrome"],"prefix":"10.1177","volume":"92","author":[{"given":"B.M","family":"Szczerba","sequence":"first","affiliation":[{"name":"Division of Nephrology, Center for Immunity Inflammation and Regenerative Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.D","family":"Rybakowska","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Immunity Inflammation and Regenerative Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Dey","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Immunity Inflammation and Regenerative Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.M.","family":"Payerhin","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Immunity Inflammation and Regenerative Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.B.","family":"Peck","sequence":"additional","affiliation":[{"name":"Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Bagavant","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Immunity Inflammation and Regenerative Medicine"},{"name":"Department of Pharmacology, University of Virginia, HSC, Box 800746, Charlottesville, VA 22908, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"U.S.","family":"Deshmukh","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Center for Immunity Inflammation and Regenerative Medicine"},{"name":"Department of Pharmacology, University of Virginia, HSC, Box 800746, Charlottesville, VA 22908, 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