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Janus kinases (JAKs) are intracellular tyrosine kinases which play a key role in the signal pathways of many cytokines, such as type l interferons (IFNs), interleukin-6 (IL-6), IL-12 and IL-23.1 All these cytokines participate in the pathogenesis of systemic lupus erythematosus (SLE). Hence, inhibition of JAK signals has provided an attractive therapeutic option in SLE. Tofacitinib can inhibit JAK1/JAK3 and has been proved effective in rheumatoid arthritis (RA),2 psoriatic arthritis and ulcerative colitis. Evidence in murine lupus have shown that tofacitinib can decrease the levels of anti-double-stranded (ds) DNA and proteinuria, remit nephritis and skin rash.3 A case report proved that tofacitinib could decrease anti-dsDNA levels in inactive SLE complicated by RA.4 A phase II randomised controlled trial reported modest efficacy of a JAK1/2 inhibitor, baricitinib, in ameliorating lupus arthritis.5
To better understand the efficacy of tofacitinib in SLE, we describe, to our knowledge for the first time, the efficacy of tofacitinib 5 mg …
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