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U.S.A."],"published-print":{"date-parts":[[2015,12,8]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    The present study is, to our knowledge, the first demonstration of the molecular mechanisms underlying the association of IFN regulatory factor 5 (IRF5) expression with milder clinical manifestations of systemic sclerosis (SSc). It is speculated that endogenous ligands induce Toll-like receptor 4 signaling and promote IRF5 transcriptional regulation of its target gene promoters, which may be required for the development of SSc. Our present study supports this notion. Symptoms associated with SSc in humans were suppressed in mice deficient in the\n                    <jats:italic>Irf5<\/jats:italic>\n                    gene. 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