{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T07:10:55Z","timestamp":1791443455936,"version":"4.3.3"},"reference-count":50,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2007,10,29]],"date-time":"2007-10-29T00:00:00Z","timestamp":1193616000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2007,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Systemic lupus erythematosus (SLE) is diagnosed according to a spectrum of clinical manifestations and autoantibodies associated with abnormal expression of type I interferon (IFN\u2010I)\u2013stimulated genes (ISGs). The role of IFN\u2010I in the pathogenesis of SLE remains uncertain, partly due to the lack of suitable animal models. The objective of this study was to examine the role of IFN\u2010I signaling in the pathogenesis of murine lupus induced by 2,6,10,14\u2010tetramethylpentadecane (TMPD).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>IFN\u2010I receptor\u2013deficient (IFNAR<jats:sup>\u2212\/\u2212<\/jats:sup>) 129Sv mice and wild\u2010type (WT) 129Sv control mice were treated intraperitoneally with TMPD. The expression of ISGs was measured by real\u2010time polymerase chain reaction. Autoantibody production was evaluated by immunofluorescence and enzyme\u2010linked immunosorbent assay. Proteinuria and renal glomerular cellularity were measured and renal immune complexes were examined by immunofluorescence.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Increased ISG expression was observed in the peripheral blood of TMPD\u2010treated WT mice, but not in the peripheral blood of TMPD\u2010treated IFNAR<jats:sup>\u2212\/\u2212<\/jats:sup> mice. TMPD did not induce lupus\u2010specific autoantibodies (anti\u2010RNP, anti\u2010Sm, anti\u2013double\u2010stranded DNA) in IFNAR<jats:sup>\u2212\/\u2212<\/jats:sup> mice, whereas 129Sv controls developed these specificities. Although glomerular immune complexes were present in IFNAR<jats:sup>\u2212\/\u2212<\/jats:sup> mice, proteinuria and glomerular hypercellularity did not develop, whereas these features of glomerulonephritis were found in the TMPD\u2010treated WT controls. The clinical and serologic manifestations observed in TMPD\u2010treated mice were strongly dependent on IFNAR signaling, which is consistent with the association of increased expression of ISGs with lupus\u2010specific autoantibodies and nephritis in humans.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Similar to its proposed role in human SLE, signaling via the IFNAR is central to the pathogenesis of autoantibodies and glomerulonephritis in TMPD\u2010induced lupus. This lupus model is the first animal model shown to recapitulate the \u201cinterferon signature\u201d in peripheral blood.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.23023","type":"journal-article","created":{"date-parts":[[2007,10,29]],"date-time":"2007-10-29T15:54:59Z","timestamp":1193673299000},"page":"3770-3783","source":"Crossref","is-referenced-by-count":165,"title":["Deficiency of the type I interferon receptor protects mice from experimental lupus"],"prefix":"10.1002","volume":"56","author":[{"given":"Dina C.","family":"Nacionales","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kindra M.","family":"Kelly\u2010Scumpia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pui Y.","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason 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