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Analysis of the expression of genes with risk alleles in cells of hematopoietic origin demonstrates them to be most abundantly expressed in B cells and dendritic cells (<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s), suggesting that these cell types may be the drivers of the inflammatory changes seen in <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s are of particular interest as they act to connect the innate and the adaptive immune response. Thus, <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s can transform inflammation into autoimmunity, and autoantibodies are the hallmark of <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>. In this review, we focus on mechanisms of tolerance that maintain <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s in a non\u2010activated, non\u2010immunogenic state. We demonstrate, using examples from our own studies, how alterations in <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> function stemming from either <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\u2010intrinsic abnormalities or <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\u2010extrinsic regulators of function can predispose to autoimmunity.<\/jats:p>","DOI":"10.1111\/imr.12348","type":"journal-article","created":{"date-parts":[[2015,12,19]],"date-time":"2015-12-19T07:39:36Z","timestamp":1450510776000},"page":"100-117","source":"Crossref","is-referenced-by-count":20,"title":["<scp>SLE<\/scp>\u2010associated risk factors affect <scp>DC<\/scp> function"],"prefix":"10.1111","volume":"269","author":[{"given":"Myoungsun","family":"Son","sequence":"first","affiliation":[{"name":"The Feinstein Institute for Medical Research Center for Autoimmune and Musculoskeletal Diseases Manhasset NY 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