ReviewFrontiers in immunology2025
Aberrant B cell responses as drivers of autoantibody generation and epitope diversification in SLE pathogenesis.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global research landscape and emerging trends of tertiary lymphoid structures in autoimmune diseases: a bibliometric analysis.Frontiers in immunology · 2026Pooled it
- Immune Repertoire Profiling Reveals Distinct Adaptive Immune Signatures of Dampness ZHENG Across Psoriasis, Rheumatoid Arthritis and Ulcerative Colitis.Cell proliferation · 2026Article
- How Epstein Barr virus shapes lupus autoimmunity: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2026Review
- mFrontiers in immunology · 2026Review
- Autoimmune nodopathy associated with Sjögren's disease and nephrotic syndrome: a case report and literature review.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.