{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T17:57:47Z","timestamp":1793383067180,"version":"4.5.0"},"reference-count":89,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T00:00:00Z","timestamp":1767916800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease characterised by loss of tolerance, widespread immune dysregulation, and production of diverse autoantibodies (typically directed against nuclear components). A central mechanism underlying this diversification of autoantibodies is epitope spreading, where immune responses directed against primary antigen-derived epitope progressively evolve to recognise additional epitopes, thereby perpetuating autoimmune pathology. Evidence from murine models and longitudinal human studies demonstrate that autoreactive B cells are central to this process, functioning both as antibody producers and antigen-presenting cells that sustain T cell responses. Special pockets within secondary lymphoid organs such as extrafollicular regions and germinal centres are the breeding ground for autoreactive B cell repertoire diversification, while tertiary lymphoid structures (TLS) provide tissue-specific niches for\n                    <jats:italic>in situ<\/jats:italic>\n                    diversification, particularly in lupus nephritis and cutaneous lupus. These aberrant B cell responses not only perpetuate autoantibody production but also shape organ-specific pathology. From a therapeutic perspective, rituximab and other anti-CD20 monoclonal antibody therapies deplete circulating B cells but may fail to eliminate plasma cells or fully dismantle TLS, allowing diversification to persist and disease relapses to occur. Early-phase studies of CD19-directed CAR-T therapy has shown potent depletion of na\u00efve and memory B cells with partial reconstitution of predominantly na\u00efve repertoires; however, long-lived plasma cells (LLPCs) and certain pathogenic subsets remain unaffected, leaving the potential for relapse. Dual-target CD19\/BCMA CAR-T approaches overcome these limitations by additionally depleting plasma cells, eliminating pre-existing autoreactive clones, and reducing inflammatory pathways, offering a more comprehensive reset of B-cell-driven autoimmunity. Epitope spreading thus represents both a driver of chronic autoimmunity and a therapeutic target, highlighting the need for interventions that precisely disrupt autoreactive B-cell networks while preserving immune function.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2025.1731285","type":"journal-article","created":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T06:36:15Z","timestamp":1767940575000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":12,"title":["Aberrant B cell responses as drivers of autoantibody generation and epitope diversification in SLE 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