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Targeting CD38 with Daratumumab in Refractory Systemic Lupus Erythematosus
Lennard Ostendorf1, Marie Burns1, Pawel Durek1
1From the Departments of Rheumatology and Clinical Immunology (L.O., P.G., R.B., U.S., G.B., F. Hiepe, T.A.), Nephrology and Internal Intensive Care Unit (P.E.), Hematology, Oncology and Tumor Immunology (U.R.), and Cardiology and Angiology, Campus Mitte (F.K.), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Deutsches Rheuma-Forschungszentrum (DRFZ) Institute of the Leibniz Association (L.O., M.B., P.D., G.A.H., F. Heinrich, A.R., H.E.M., M.-F.M., F. Hiepe, T.A.), German Center for Cardiovascular Research (DZHK) (F.K.), and BIH Brandenburg Center for Regenerative Therapies (BCRT), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin (M.-F.M.) - all in Berlin; and the Laboratory of Inflammation and Autoimmunity, Biomedical Research Foundation, Academy of Athens, Athens (P.G.).
Abstract:
Daratumumab, a human monoclonal antibody that targets CD38, depletes plasma cells and is approved for the treatment of multiple myeloma. Long-lived plasma cells are implicated in the pathogenesis of systemic lupus erythematosus because they secrete autoantibodies, but they are unresponsive to standard immunosuppression. We describe the use of daratumumab that induced substantial clinical responses in two patients with life-threatening lupus, with the clinical responses sustained by maintenance therapy with belimumab, an antibody to B-cell activating factor. Significant depletion of long-lived plasma cells, reduction of interferon type I activity, and down-regulation of T-cell transcripts associated with chronic inflammation were documented. (Supported by the Deutsche Forschungsgemeinschaft and others.).
