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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 …
Handling editor Josef S Smolen
HY and GZ contributed equally.
Funding This work was supported by the Chinese National Key Research R&D Program (grant number 2017YFC0907601, 2017YFC0907602, 2017YFC0907603, 2008BAI59B02) and the Chinese National High Technology Research and Development Program, Ministry of Science and Technology (grant number2012AA02A513).
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval Approved by the Ethics Committee of Peking Union Medical College Hospital.
Provenance and peer review Not commissioned; externally peer reviewed.
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