ArticleThe American journal of pathology2004
B Lymphocyte signaling established by the CD19/CD22 loop regulates autoimmunity in the tight-skin mouse.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 87 citations in OpenAlex.
- B-cell depletion therapy in patients with diffuse systemic sclerosis associates with a significant decrease in PDGFR expression and activation in spindle-like cells in the skin.Arthritis research & therapy · 2012Trial
- Experience with rituximab in scleroderma: results from a 1-year, proof-of-principle study.Rheumatology (Oxford, England) · 2010Trial
- B cell depletion in diffuse progressive systemic sclerosis: safety, skin score modification and IL-6 modulation in an up to thirty-six months follow-up open-label trial.Arthritis research & therapy · 2010Trial
- Roles of TRIM21/Ro52 in connective tissue disease-associated interstitial lung diseases.Frontiers in immunology · 2024Review
- Autoantibodies as Biomarker and Therapeutic Target in Systemic Sclerosis.Biomedicines · 2022Review
- Therapeutic Options for Systemic Sclerosis: Current and Future Perspectives in Tackling Immune-Mediated Fibrosis.Biomedicines · 2022Review
- Dysregulated B cell function and disease pathogenesis in systemic sclerosis.Frontiers in immunology · 2022Review
- Role of B-Cell in the Pathogenesis of Systemic Sclerosis.Frontiers in immunology · 2022Review
- The Role of B Cells in Scleroderma Lung Disease Pathogenesis.Frontiers in medicine · 2022Review
- B cells in systemic sclerosis: from pathophysiology to treatment.Clinical rheumatology · 2021Review
- The target on B cells in Systemic Sclerosis: a "midsummer dream" to extinguish inflammation and prevent early disease progression to fibrosis.Clinical rheumatology · 2021Article
- A 3-Year Observational Study of Patients with Progressive Systemic Sclerosis Treated with an Intensified B Lymphocyte Depletion Protocol: Clinical and Immunological Response.Journal of clinical medicine · 2021Article
- The Roles of Immune Cells in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2020Review
- Inhibition of effector B cells by ibrutinib in systemic sclerosis.Arthritis research & therapy · 2020Article
- Emerging targets of disease-modifying therapy for systemic sclerosis.Nature reviews. Rheumatology · 2019Review
- The immunopathogenesis of fibrosis in systemic sclerosis.Clinical and experimental immunology · 2019Review
- Decreased CD22 expression and intracellular signaling aberrations in B cells of patients with systemic sclerosis.Rheumatology international · 2018Article
- Challenges and opportunities in treating inflammation associated with pulmonary hypertension.Expert review of cardiovascular therapy · 2016Review
- Abnormal B lymphocyte activation and function in systemic sclerosis.Annals of dermatology · 2015Review
- Systemic Sclerosis Patients Present Alterations in the Expression of Molecules Involved in B-Cell Regulation.Frontiers in immunology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Systemic sclerosis (SSc) is characterized by fibrosis and autoimmmunity. Peripheral blood B cells from SSc patients specifically overexpress CD19, a critical cell-surface signal transduction molecule in B cells. CD19 deficiency in B cells also attenuates skin fibrosis in the tight-skin (TSK/+) mouse, a genetic model for SSc. Herein we analyzed two transgenic mouse lines that overexpress CD19. Remarkably, 20% increase of CD19 expression in mice spontaneously induced SSc-specific anti-DNA topoisomerase I (topo I) antibody (Ab) production, which was further augmented by 200% overexpression. In TSK/+ mice overexpressing CD19, skin thickness did not increase, although anti-topo I Ab levels were significantly augmented, indicating that abnormal CD19 signaling influences autoimmunity in TSK/+ mice and also that anti-topo I Ab does not have a pathogenic role. The molecular mechanisms for abnormal CD19 signaling were further assessed. B-cell antigen receptor crosslinking induced exaggerated calcium responses and augmented activation of extracellular signal-regulated kinase in TSK/+ B cells. CD22 function was specifically impaired in TSK/+ B cells. Consistently, CD19, a major target of CD22-negative regulation, was hyperphosphorylated in TSK/+ B cells. These findings indicate that reduced inhibitory signal provided by CD22 results in abnormal activation of signaling pathways including CD19 in TSK/+ mice and also suggest that this disrupted B cell signaling contribute to specific autoantibody production.
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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.