Abstract

In systemic lupus erythematosus (SLE), the interaction between hyperactive T cells and B cells causes a dysregulated production of autoantibodies that can lead to tissue damage and impaired organ function. Studies on the modalities of communication between T and B cells have led to the design of new therapeutics for SLE, including autoantibodyderived peptide immunotherapies. Since many autoantibodies in SLE patients have amino acid sequences similar to those of murine antibodies, and at similar locations, the current directions are to employ strategies that have given promising results in mice in human clinical settings. This review describes the experimental evidence, rationale, and preclinical models of autoantibody-derived peptide immunotherapy in SLE, and how this information is translating into clinical studies in humans.