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Emerging evidences suggested that defects of sphingolipid metabolism were responsible for <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content> pathogenesis. However, it is not clear whether these defects exist in B cells and macrophages under <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content> condition and whether <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content> signalling pathway was related to the dysfunction of sphingolipid metabolism in <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>. Here, we demonstrated that the enzymes involved in the sphingolipid metabolism expressed abnormally in B cells from <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content> patients and lupus\u2010prone mice. Moreover, we found that <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content> signalling induced the abnormal expression of sphingomyelin phosphodiesterase 3 (<jats:styled-content style=\"fixed-case\">SMPD<\/jats:styled-content>3), sphingosine\u20101\u2010phosphate phosphatase 2 (<jats:styled-content style=\"fixed-case\">SGPP<\/jats:styled-content>2), ceramide kinase (<jats:styled-content style=\"fixed-case\">CERK<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">UDP<\/jats:styled-content> glycosyltransferase 8 (<jats:styled-content style=\"fixed-case\">UGT<\/jats:styled-content>8), which were involved in sphingolipid metabolism. <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content> signalling also induced the transportation of <jats:styled-content style=\"fixed-case\">SMPD<\/jats:styled-content>3 from Golgi apparatus. Furthermore, the dysfunction of <jats:styled-content style=\"fixed-case\">SMPD<\/jats:styled-content>3 enhanced <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\u2010induced inflammatory response of B cells and macrophages in turn. Thus, these findings provide an innovative direction and a new target for research and treatment of <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/sji.12611","type":"journal-article","created":{"date-parts":[[2017,9,10]],"date-time":"2017-09-10T11:22:37Z","timestamp":1505042557000},"page":"377-388","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["<scp>TLR<\/scp>\u2010Induced <scp>SMPD<\/scp>3 Defects Enhance Inflammatory Response of B Cell and Macrophage in the Pathogenesis of <scp>SLE<\/scp>"],"prefix":"10.1111","volume":"86","author":[{"given":"F.","family":"Liu","sequence":"first","affiliation":[{"name":"The State Key Laboratory of Pharmaceutical Biotechnology Division of Immunology Medical School Nanjing University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"X.","family":"Li","sequence":"additional","affiliation":[{"name":"The 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