ArticleJournal of biomedicine & biotechnology2012
Comprehensive evaluation of different T-helper cell subsets differentiation and function in rheumatoid arthritis.
Article in Journal of biomedicine & biotechnology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses 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
28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- Review: progression and heterogeneity of multiple sources of mesenchymal stromal cells for the treatment of rheumatoid arthritis.Stem cell research & therapy · 2025Pooled it
- The Proportion of Regulatory T Cells in Patients with Rheumatoid Arthritis: A Meta-Analysis.PloS one · 2016Pooled it
- The Sufficient Immunoregulatory Effect of Autologous Bone Marrow-Derived Mesenchymal Stem Cell Transplantation on Regulatory T Cells in Patients with Refractory Rheumatoid Arthritis.Journal of immunology research · 2020Trial
- IL-6 Mediated Transcriptional Programming of Naïve CD4+ T Cells in Early Rheumatoid Arthritis Drives Dysregulated Effector Function.Frontiers in immunology · 2019Trial
- JAK/STAT inhibition reprograms T cell activation and metabolism in inflammatory arthritis patients.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Comparison of inflammatory molecular mechanisms between osteoarthritis and rheumatoid arthritis via gene microarrays.Molecular biology research communications · 2024Article
- Cell-specific gene networks and drivers in rheumatoid arthritis synovial tissues.Frontiers in immunology · 2024Article
- Characteristics of the Gut Microbiome and Its Relationship With Peripheral CD4Frontiers in microbiology · 2022Article
- The regulation of T helper cell polarization by the diterpenoid fraction ofFrontiers in pharmacology · 2022Article
- Reestablish immune tolerance in rheumatoid arthritis.Frontiers in immunology · 2022Review
- Cancer and Autoimmune Diseases: A Tale of Two Immunological Opposites?Frontiers in immunology · 2022Article
- Reduction of Oxidative Stress in Peripheral Blood Mononuclear Cells Attenuates the Inflammatory Response of Fibroblast-like Synoviocytes in Rheumatoid Arthritis.International journal of molecular sciences · 2021Article
- Immunologic Parameters for Disease Activity in Rheumatoid Arthritis.Archives of Razi Institute · 2021Article
- Effects of Biological Therapies on Molecular Features of Rheumatoid Arthritis.International journal of molecular sciences · 2020Review
- Update on the Pathomechanism, Diagnosis, and Treatment Options for Rheumatoid Arthritis.Cells · 2020Review
- Regulation of T Cell Activities in Rheumatoid Arthritis by the Novel Fusion Protein IgD-Fc-Ig.Frontiers in immunology · 2020Article
- Intracytoplasmic Expression of IL-6 and IL-17A in Circulating CD4+ T Cells Are Strongly Associated with and Predict Disease Activity in Rheumatoid Arthritis: A Case-Control Study in Ghana.International journal of rheumatology · 2020Article
- Effect of tumor necrosis factor inhibition on spinal inflammation and spinal ankylosis in SKG mice.Scientific reports · 2019Article
- High-throughput RNA sequencing reveals distinct gene signatures in active IgG4-related disease.Scientific reports · 2017Article
- Involvement of the IL-23/IL-17 axis and the Th17/Treg balance in the pathogenesis and control of autoimmune arthritis.Cytokine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is the most common autoimmune disorder. Loss of Th1/Th2 and Th17/Treg balance has been reported in several inflammatory autoimmune diseases. This study was to investigate Th1, Th2, Th17, and Treg differentiation and related cytokines in RA patients. The frequencies of Th1, Th2, Th17, and Treg cells in peripheral blood of RA patients (n = 76) and healthy controls (n = 18) were determined by flow cytometry. Eight serum cytokines were analyzed using cytometric bead array. The results demonstrated that RA patients exhibited increased peripheral Th1/Th17 cells and Th1/Th17-related cytokines. However, Th1 cells only reached significant difference at advanced stage, but Th17 at all stages, suggesting more important roles in Th17 cells. For Th2 and Treg cells, there was a different function pattern in RA progression. Although with the increase of DAS28 score, Th2 cell experienced some degree of decrease in RA patients, no significant difference was observed. IL-4 and IL-10 showed a significant increase in RA patients. These indicated that Th2 cells might exert immunosuppression effects mainly by secreting cytokines. Treg cells were found significantly decreased in RA patients, but no difference was observed in TGF-β expression, indicating a cell-cell interaction pattern in Treg cell.
Indexed as
Identifiers
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.