ArticleArthritis research & therapy2009
CTLA4-Ig interacts with cultured synovial macrophages from rheumatoid arthritis patients and downregulates cytokine production.
Article in Arthritis research & therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03215927 (A Randomized, Controlled Pilot Trial to Evaluate the Efficacy and Safety of Subcutaneous Abatacept in Treating Interstitial Lung Disease Associated With the Anti-synthetase Syndrome), which is not on this map. Cited by 34 papers, 2 of them syntheses that pooled it.
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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.
A Randomized, Controlled Pilot Trial to Evaluate the Efficacy and Safety of Subcutaneous Abatacept in Treating Interstitial Lung Disease Associated With the Anti-synthetase Syndrome
Who cites it
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.
- Association betweenAging · 2021Pooled it
- Genome-Wide Association Meta-Analysis Reveals Novel Juvenile Idiopathic Arthritis Susceptibility Loci.Arthritis & rheumatology (Hoboken, N.J.) · 2017Pooled it
- Genetic Variations inGenes · 2026Article
- CTLA4-Ig reduces proliferation and inflammatory gene expression in muscle fibroblasts, corresponding to less fibrosis and inflammation inAmerican journal of physiology. Cell physiology · 2026Article
- Immune checkpoint inhibitor-related arthritis and oral disorders: shared pathophysiology and clinical implications for rheumatology and oral health.Cancer cell international · 2025Review
- Dynamic macrophage phenotypes in autoimmune and inflammatory rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- Molecular mechanism of quercetin in treating RA-ILD based on network pharmacology, molecular docking, and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Crosstalk between efferocytic myeloid cells and T-cells and its relevance to atherosclerosis.Frontiers in immunology · 2024Review
- Efficacy of COVID-19 mRNA vaccination in patients with autoimmune disorders: humoral and cellular immune response.BMC medicine · 2023Article
- New insights into inflammatory osteoclast precursors as therapeutic targets for rheumatoid arthritis and periodontitis.Bone research · 2023Review
- Multiple Shades of Gray-Macrophages in Acute Allograft Rejection.International journal of molecular sciences · 2023Review
- Past, Present, and Future in Dermatomyositis Therapeutics.Current treatment options in rheumatology · 2022Article
- Abatacept downregulates Fcγ receptor I on circulating monocytes: a potential therapeutic mechanism in patients with rheumatoid arthritis.Arthritis research & therapy · 2022Article
- Repolarization of Unbalanced Macrophages: Unmet Medical Need in Chronic Inflammation and Cancer.International journal of molecular sciences · 2022Review
- Co-Inhibitory Molecules - Their Role in Health and Autoimmunity; Highlighted by Immune Related Adverse Events.Frontiers in immunology · 2022Review
- The Role of M1/M2 Macrophage Polarization in Rheumatoid Arthritis Synovitis.Frontiers in immunology · 2022Review
- CTLA4-Ig treatment induces M1-M2 shift in cultured monocyte-derived macrophages from healthy subjects and rheumatoid arthritis patients.Arthritis research & therapy · 2021Article
- In vitro effect of biological and conventional disease-modifying antirheumatic drugs on fibrocyte differentiation in patients with rheumatoid arthritis and healthy controls.European journal of rheumatology · 2021Article
- Cytotoxic T lymphocyte-associated antigen-4-Ig (CTLA-4-Ig) suppresses Staphylococcus aureus-induced CD80, CD86, and pro-inflammatory cytokine expression in human B cells.Arthritis research & therapy · 2020Article
- Immune checkpoint inhibitor-induced inflammatory arthritis as a model of autoimmune arthritis.Immunological reviews · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCo-stimulatory signal B7(CD80/CD86):CD28 is needed in order to activate T cells in immune response. Cytotoxic T lymphocyte-associated antigen-4-immunoglobulin (CTLA4-Ig) binding to the B7 molecules on antigen-presenting cells downregulates this activation and represents a recent biological treatment in rheumatoid arthritis (RA). Objectives of the study were to investigate the presence of the B7.2 (CD86) molecule and its masking by CTLA4-Ig on cultures of both RA synovial macrophages (RA SM), and of macrophages differentiated from THP-1 cells (M). In addition, the anti-inflammatory effects of CTLA4-Ig on co-cultures of RA SM and M with activated T cells were tested.
methodsAll macrophages were co-cultured for 24 hours with activated T cells, without or with CTLA4-Ig (10, 100, 500 microg/ml for 1 hour, 3 hours and overnight, respectively). Immunofluorescence (IF) staining for B7.2, and an analysis of inflammatory cytokine expression (interleukin (IL) -6, tumor necrosis factor (TNF) alpha, IL-1beta, transforming growth factor (TGF) beta) by immunocytochemistry (ICC), western blot (WB) and reverse transcriptase-polymerase chain reaction (RT-PCR) were performed.
resultsMacrophages showed intense B7.2 expression. CTLA4-Ig/B7.2 masking was evident for all macrophages, even after only 1 hour of cell culture (range from 10 to 100 microg/ml). ICC of co-cultures showed a dose-dependent decrease in inflammatory cytokines (P < 0.001 for IL-6, TNFalpha, IL-1beta and TGFbeta). Data were confirmed by WB and RT-PCR analysis.
conclusionsOptimal concentrations of CTLA4-Ig for the CTLA4-Ig/B7.2 masking on activated macrophages were identified and were found to induce significant downregulation in the cell production of IL-6, TNFalpha, IL1-beta and TGFbeta. In conclusion, macrophages would appear to be a sensitive target for CTLA4-Ig treatment in RA.
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