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Systemic lupus erythematosus (SLE) is an autoimmune disease induced by autoreactive T cell activation and B cell autoantibody overproduction. The efficacy of rituximab in refractory SLE has been documented, although some patients show partial response only.1,–,9 We report here two patients with SLE who showed T cell-dominant flare-up and two others who showed B cell-dependent flare-up, after long-term remission induced by rituximab administered at 375 mg/m2 twice/week.
Rituximab rapidly depleted peripheral naive and memory B cells in patients with SLE. Patients with prolonged remission had persistent depletion of memory B cells for >2 years, whereas recovery of naive B cells occurred within 3–9 months. The expression levels of CD80 on B cells diminished rapidly and remained downregulated. Furthermore, CD69 and ICOS (inducible T-cell co-stimulator) expression levels on CD4+ T cells also decreased and remained at low levels.10
B cell-dominant recurrence occurred in two patients, who were concurrently positive for anti-ds-DNA antibodies and extractable nuclear antigen, with lupus nephritis (class II) before treatment …
Competing interests YT has received consulting fees, speaking fees and/or honoraria from Mitsubishi-Tanabe Pharma, Chugai Pharma, Eisai Pharma, Pfizer, Abbott Immunology Pharma, Daiichi-Sankyo, Janssen Pharma, Astra-Zeneca, Takeda Industrial Pharma, Astellas Pharma, Asahi-kasei Pharma and GlaxoSmithKline and has received research grant support from Mitsubishi-Tanabe Pharma, Bristol-Myers Squibb, Takeda Industrial Pharma, MSD, Astellas Pharma, Eisai Pharma, Chugai Pharma, Pfizer and Daiichi-Sankyo. The other authors declare no conflict of interest.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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