{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T21:07:52Z","timestamp":1777928872151,"version":"3.51.4"},"reference-count":49,"publisher":"SAGE Publications","issue":"14","license":[{"start":{"date-parts":[[2020,9,22]],"date-time":"2020-09-22T00:00:00Z","timestamp":1600732800000},"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":["Lupus"],"published-print":{"date-parts":[[2020,12]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>The feed-forward loop of type I interferons (IFNs) production and subsequent immunopathology of systemic lupus erythematosus (SLE) has been hypothesised to be disrupted with inhibition of IFN\u03b1 or type I IFN receptor subunit 1 (IFNAR). This systematic review and meta-analysis present the treatment efficacy and safety profile of monoclonal antibodies inhibiting IFN\u03b1 or IFNAR.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A search was done using Medline, Embase and ClinicalTrials.gov for biologics targeting IFN\u03b1 or IFNAR in SLE up to 3 Jan 2020. For the meta-analysis, analyses of binary variables were pooled using odds ratio (OR) with the Mantel Haenszel model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Anifrolumab 300 mg (n\u2009=\u20093 studies, 927 patients) was more effective than placebo in achieving SRI(4) (pooled OR\u2009=\u20091.91, CI 1.11-3.28, P\u2009=\u20090.02) and BICLA response (pooled OR\u2009=\u20092.25, CI 1.72-2.95, P\u2009&lt;\u20090.00001). In SLE patients with high type I IFN gene signature, SRI(4) response was not achieved with anifrolumab in 2 studies, 450 patients. Treatment with IFN\u03b1 and IFNAR inhibitors (n\u2009=\u20097 studies, 1590 patients) increased the risk of herpes zoster infection (pooled OR\u2009=\u20093.72, CI 1.88\u20137.39, P\u2009=\u20090.0002), upper respiratory tract infections, nasopharyngitis and bronchitis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This meta-analysis substantiates IFNAR as a therapeutic target in SLE. Inhibition of type I IFNs predisposes to herpes zoster and other viral infections.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/0961203320959702","type":"journal-article","created":{"date-parts":[[2020,9,22]],"date-time":"2020-09-22T18:31:42Z","timestamp":1600799502000},"page":"1845-1853","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":18,"title":["Biologics targeting type I interferons in SLE: A meta-analysis and systematic review of randomised controlled trials"],"prefix":"10.1177","volume":"29","author":[{"given":"Jeffery Wei Heng","family":"Koh","sequence":"first","affiliation":[{"name":"Department of Pharmacy, Faculty of Science, National University of Singapore, Singapore, Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cheng Han","family":"Ng","sequence":"additional","affiliation":[{"name":"Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7907-5288","authenticated-orcid":false,"given":"Sen Hee","family":"Tay","sequence":"additional","affiliation":[{"name":"Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore"},{"name":"Division of Rheumatology, Department of Medicine, National University Hospital, Singapore, Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2020,9,22]]},"reference":[{"key":"bibr1-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1177\/0961203317693096"},{"key":"bibr2-0961203320959702","first-page":"S126","volume":"29","author":"Mosca M","year":"2011","journal-title":"Clin Exp Rheumatol"},{"key":"bibr3-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1093\/rheumatology\/keaa002"},{"key":"bibr4-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1111\/j.1479-8077.2006.00229.x"},{"key":"bibr5-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1038\/nrrheum.2009.237"},{"key":"bibr6-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM197907053010102"},{"key":"bibr7-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2006.08.010"},{"key":"bibr8-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1126\/science.1064890"},{"key":"bibr9-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1186\/ar3206"},{"key":"bibr10-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1002\/art.20254"},{"key":"bibr11-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1002\/art.37824"},{"key":"bibr12-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2007.074765"},{"key":"bibr13-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1177\/0961203309105529"},{"key":"bibr14-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1186\/s12920-018-0468-1"},{"key":"bibr15-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1002\/art.39962"},{"key":"bibr16-0961203320959702","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.l4898"},{"key":"bibr17-0961203320959702","doi-asserted-by":"crossref","unstructured":"McGuinness LA and Higgins JPT. 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