ArticleJCI insight2023
Autoreactive B cells in rheumatoid arthritis include mainly activated CXCR3+ memory B cells and plasmablasts.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- CD19 CAR T cell therapy for treatment-refractory seropositive rheumatoid arthritis: a phase 1 trial.Nature medicine · 2026Article
- Anti-Modified Protein Antibodies in Rheumatoid Arthritis: Pathogenic, Protective, or Passive Bystander?Immunological reviews · 2026Review
- The Developmental and Functional Implications of Age-Associated B Cells (ABCs) Across Tissue Microenvironments.Immunological reviews · 2026Review
- B cell-intrinsic CXCR3 drives efficient generation of ectopic pulmonary germinal center responses to influenza A virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Rheumatoid arthritis developing after mogamulizumab treatment in Sézary syndrome.EULAR rheumatology open · 2026Article
- Roads and detours for CAR T cell therapy in autoimmune diseases.Nature reviews. Drug discovery · 2026Review
- CXCR3 expression on antigen-experienced B cells is systemically dysregulated in type 1 diabetes.Diabetologia · 2026Article
- Revisiting B-cell targeted therapies in rheumatoid arthritis: from paradoxical biology to deep immune reset.Frontiers in immunology · 2026Review
- Biosafety assessment of engineered CCL20 locked dimers in vivo.Cell biology and toxicology · 2025Article
- Distinct autoreactive CD19Nature communications · 2025Article
- Article
- Pathogenic Role of Cytokines in Rheumatoid Arthritis.Journal of clinical medicine · 2025Review
- Chimeric Antigen Receptor T Cell Immunotherapy for Autoimmune Rheumatic Disorders: Where Are We Now?Cells · 2025Review
- Current state and future directions of basic research in rheumatoid arthritis.Journal of rheumatic diseases · 2025Review
- The regulatory functions of G protein-coupled receptors signaling pathways in B cell differentiation and development contributing to autoimmune diseases.Cell & bioscience · 2025Review
- Review
- Fluorescent probes in autoimmune disease research: current status and future prospects.Journal of translational medicine · 2025Review
- Age-Associated B Cells in Autoimmune Diseases: Pathogenesis and Clinical Implications.Clinical reviews in allergy & immunology · 2025Review
- B Cell Receptor Repertoire Analysis of the CD21European journal of immunology · 2025Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many autoimmune diseases (AIDs) are characterized by the persistence of autoreactive B cell responses, which have been directly implicated in disease pathogenesis. How and why these cells are generated or how they are maintained for years is largely unknown. Rheumatoid arthritis (RA) is among the most common AIDs and is characterized by autoantibodies recognizing proteins with posttranslational modifications (PTMs). This PTM-directed autoreactive B cell compartment is ill defined. Here, we visualized the B cell response against the three main types of PTM antigens implicated in RA by spectral flow cytometry. Our results showed extensive cross-reactivity of PTM-directed B cells against all three PTM antigens (citrulline, homocitrulline, and acetyllysine). Unsupervised clustering revealed several distinct memory B cell (mBC) populations. PTM-directed cells clustered with the most recently activated class-switched mBC phenotype, with high CD80, low CD24, and low CD21 expression. Notably, patients also harbored large fractions of PTM-directed plasmablasts (PBs). Both PTM-directed mBCs and PBs showed high expression of CXCR3, a receptor for chemokines present in abundance in arthritic joints. Together, our data provide detailed insight into the biology of B cell autoreactivity and its remarkable, seemingly exhaustless persistence in a prominent human AID.
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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.