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Purpose Programmed death ligand 1 (PD-L1) plays an important role in controlling autoreactive and follicular T helper lymphocytes, which can induce autoantibody production. Properly expressed PD-L1 thus prevents autoimmune disease. Induced by inflammatory cytokines, PD-L1 is elevated on monocytes from patients with infections and rheumatoid arthritis, but is poorly expressed on monocytes from SLE patients with active disease. Our goal was to define the mechanism for PD-L1 dysregulation in pediatric patients with SLE, and to clinically characterize those patients with loss of PD-L1.

PD-L1 expression on monocytes marks active systemic lupus erythematosus in patients without nephritis