ArticleThe Journal of clinical investigation2001
Fibroblast-like synoviocytes support B-cell pseudoemperipolesis via a stromal cell-derived factor-1- and CD106 (VCAM-1)-dependent mechanism.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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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.
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Who cites it
74 citing papers in PubMed, 178 citations in OpenAlex.
- Adipose-Joint Crosstalk in Obesity-Induced Osteoarthritis: Mechanisms, Biomarkers, and Translational Therapeutic Opportunities.Current rheumatology reports · 2026Review
- The Developmental and Functional Implications of Age-Associated B Cells (ABCs) Across Tissue Microenvironments.Immunological reviews · 2026Review
- Age-Associated B Cells: Origins, Regulation, and Tissue-Specific Pathogenic Contributions in Autoimmune, Metabolic, and Neurological Diseases.Immunological reviews · 2026Review
- Gas Plasma Exposure Attenuates the Inflammatory Rheumatoid Arthritis-Like Phenotype of Murine Synoviocytes in Vitro.Journal of cellular and molecular medicine · 2026Article
- Macrophage-centred crosstalk with infiltrating immune cells in rheumatoid arthritis and its regulation by mesenchymal stem cells.Journal of translational medicine · 2025Review
- Shelter in place: live CLL cells inside the bone marrow fibroblasts and its implication in residual disease persistence.Blood neoplasia · 2025Article
- The Role of Tumor Microenvironment and Targeted Therapy in Chronic Lymphocytic Leukemia.Current issues in molecular biology · 2025Review
- Tumor microenvironment as a novel therapeutic target for lymphoid leukemias.Annals of hematology · 2025Review
- Age-Associated B Cells in Autoimmune Diseases: Pathogenesis and Clinical Implications.Clinical reviews in allergy & immunology · 2025Review
- Lymphoid stroma in all its states.Frontiers in immunology · 2025Review
- Biomaterials for Modulating the Immune Microenvironment in Rheumatoid Arthritis.BME frontiers · 2025Review
- Targeting pathogenic fibroblast-like synoviocyte subsets in rheumatoid arthritis.Arthritis research & therapy · 2024Review
- Applications of single-cell RNA sequencing in rheumatoid arthritis.Frontiers in immunology · 2024Review
- Dihydroartemisinin Regulated the MMP-Mediated Cellular Microenvironment to Alleviate Rheumatoid Arthritis.Research (Washington, D.C.) · 2024Article
- Chronic Lymphocytic Leukemia: Disease Biology.Acta haematologica · 2024Review
- Distinct fibroblast functions associated with fibrotic and immune-mediated inflammatory diseases and their implications for therapeutic development.F1000Research · 2024Review
- The Role of the Microenvironment and Cell Adhesion Molecules in Chronic Lymphocytic Leukemia.Cancers · 2023Review
- Review
- New Insights into the Role of Synovial Fibroblasts Leading to Joint Destruction in Rheumatoid Arthritis.International journal of molecular sciences · 2023Review
- Age/autoimmunity-associated B cells in inflammatory arthritis: An emerging therapeutic target.Frontiers in immunology · 2023Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
B-cell accumulation and formation of ectopic germinal centers are characteristic changes in the diseased joints of patients with rheumatoid arthritis (RA). Earlier studies suggested that interactions between B lymphocytes and specialized synovial "nurse-like" cells peculiar to the RA synovium may be responsible for the homing and sustained survival of B cells in the synovium. However, in this study, we found that B cells spontaneously migrate beneath ordinary fibroblast-like synoviocytes (FLSs) and then experience prolonged survival. FLSs isolated from joints of patients with osteoarthritis also supported this activity, termed B-cell pseudoemperipolesis. We found that FLSs constitutively expressed the chemokine stromal cell-derived factor-1 (SDF-1), and that pertussis toxin or antibodies to the SDF-1 receptor (CXCR4) could inhibit B-cell pseudoemperipolesis. However, expression of SDF-1 is not sufficient, as dermal fibroblasts also expressed this chemokine but were unable to support B-cell pseudoemperipolesis unless previously stimulated with IL-4 to express CD106 (VCAM-1), a ligand for the alpha(4)beta(1) integrin, very-late-antigen-4 (VLA-4 or CD49d). Furthermore, mAb's specific for CD49d and CD106, or the synthetic CS1 fibronectin peptide, could inhibit B-cell pseudoemperipolesis. We conclude that ordinary FLSs can support B-cell pseudoemperipolesis via a mechanism dependent upon fibroblast expression of SDF-1 and CD106.
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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.