ArticleScientific reports2022
CTLA-4-Ig internalizes CD80 in fibroblast-like synoviocytes from chronic inflammatory arthritis mouse model.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- CTLA4-Ig reduces proliferation and inflammatory gene expression in muscle fibroblasts, corresponding to less fibrosis and inflammation inAmerican journal of physiology. Cell physiology · 2026Article
- Modulating immune response for the prevention and treatment of type 1 diabetes.Frontiers in immunology · 2026Review
- Genome-Wide Aggregated Trans Effects Analysis Identifies Genes Encoding Immune Checkpoints as Core Genes for Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Redefinition of Synovial Fibroblasts in Rheumatoid Arthritis.Aging and disease · 2024Review
- Therapeutic Efficacy of Medicinal Plants with Allopathic Medicine in Musculoskeletal Diseases.International journal of plant, animal and environmental sciences · 2024Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD80 interact with CD28 and CTLA-4 on antigen-presenting cells, and function in the co-stimulatory signaling that regulates T cell activity. CTLA-4-Ig is used to treat RA by blocking co-stimulatory signaling. Chronic inflammatory arthritis was induced in D1BC mice using low-dose arthritogenic antigens and treated with CTLA-4-Ig. We performed histopathology of the joints and lymph nodes, serological examination for rheumatoid factors, and flow cytometric analysis of isolated synovial cells, including CD45
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