Trial reportJournal of immunology (Baltimore, Md. : 1950)2019
Monocyte/Macrophage Abnormalities Specific to Rheumatoid Arthritis Are Linked to miR-155 and Are Differentially Modulated by Different TNF Inhibitors.
Trial report in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Role of miR-155 in inflammatory autoimmune diseases: a comprehensive review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Pooled it
- Review
- Inhibitory effects of spermidine on lipopolysaccharide-induced inflammation in RAW 264.7 cells.Experimental and therapeutic medicine · 2026Article
- Macrophage Cell Culture and Characterization by Serum Human AB in Health and Disease.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Aberrant STAT3 activation and overproduction of IL-21 in systemic lupus erythematosus: role of miR-155 and miR-21 in target genesFrontiers in immunology · 2026Article
- The utility of miR-16, miR-146a and miR-155 in serum and urine for juvenile idiopathic arthritis diagnostics and monitoring.Pediatric rheumatology online journal · 2025Article
- miRNAs and T cell-mediated Immune Response in Disease.The Yale journal of biology and medicine · 2025Review
- Advancing Ischemic Stroke Prognosis: Key Role of MiR-155 Non-Coding RNA.International journal of molecular sciences · 2025Review
- Healthy and premature aging of monocytes and macrophages.Frontiers in immunology · 2025Review
- Role of double-negative autoreactive cells (CD4Heliyon · 2024Article
- Review
- Article
- Nanocarrier-Mediated Delivery of MicroRNAs for Fibrotic Diseases.Molecular diagnosis & therapy · 2024Review
- MicroRNAs as Key Regulators in RA and SLE: Insights into Biological Functions.Current pharmaceutical design · 2024Review
- Regulation of Macrophage Polarization in Allergy by Noncoding RNAs.Non-coding RNA · 2023Review
- Article
- Post-transcriptional checkpoints in autoimmunity.Nature reviews. Rheumatology · 2023Review
- Role of miRNAs in Rheumatoid Arthritis Therapy.Cells · 2023Review
- Role of ceRNA network in inflammatory cells of rheumatoid arthritis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- MicroRNAs in Macrophages: Regulators of Activation and Function.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proinflammatory macrophages and miR-155 are increased in patients with rheumatoid arthritis (RA). We studied membrane TNF (mTNF) expression on blood monocytes, polarization into macrophages, miR-155 expression, and the effect of anti-TNF on these biomarkers in RA patients. Sixty-seven RA patients and 109 controls (55 healthy, 54 with spondyloarthritis and connective tissue diseases) were studied. Monocytes were isolated and differentiated into macrophages with or without anti-TNF. mTNF expression was increased on monocytes from RA patients, but not from other inflammatory diseases, correlated with disease activity. Under human serum AB or M-CSF, only monocytes from RA had a defect of differentiation into M2-like macrophages and had a propensity for preferential maturation toward M1-like macrophages that contributed to synovial inflammation. This defect was correlated to mTNF expression and was partially reversed by monoclonal anti-TNF Abs but not by the TNF soluble receptor. miR-155 was increased in M2-macrophages except in adalimumab-treated patients. Transfection of healthy monocytes with miR-155 induced a decrease in M2-like markers, and transfection of RA monocytes with antagomir-155 allowed restoration of M2-like polarization. Defect in differentiation of monocytes into M2-like-macrophages linked to increased miR-155 and correlated with increased mTNF on monocytes could play a key role in RA pathogenesis. Monoclonal anti-TNF Abs but not the TNF soluble receptor partially restored this defect.
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What OpenQuestion holds
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.