Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (807 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Rheumatoid Arthritis.
Where it fits in the MeSH classification
- Broader topics
- Arthritis; Rheumatic Diseases; Autoimmune Diseases
- Narrower topics
- Caplan Syndrome; Felty Syndrome; Rheumatoid Nodule; Rheumatoid Vasculitis; Sjogren's Syndrome; Still's Disease, Adult-Onset
Research landscape
PubMed indexes 137,387 records tagged with the MeSH heading “Arthritis, Rheumatoid” (counts retrieved 2026-10-29). 24,529 of them (17.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 56,306 records.
Reviews account for 21,203 records (15.4%) and meta-analyses for 1,718. Randomized controlled trials number 4,412 (3.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 56,306 |
| 2000-2009 | 23,941 |
| 2010-2019 | 32,611 |
| 2020 onward | 24,529 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 21,203 | 15.4% |
| Meta-analyses | 1,718 | 1.3% |
| Randomized controlled trials | 4,412 | 3.2% |
Method: PubMed query "Arthritis, Rheumatoid"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in immunology
Immune responses are studied in model organisms, in cells from donors and in patients, and the same pathway can behave differently across these settings. Mouse immune systems differ from human ones in important ways, and blood measurements may not reflect what happens in tissues. Clinical conclusions about immune-mediated disease or immunotherapy come mainly from controlled trials and long-term cohorts. Check the species and tissue studied, whether markers were linked to outcomes patients notice, and the follow-up time.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Immunological profiling of rheumatoid factor-positive primary Sjögren's syndrome by single-cell RNA sequencing | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42367820 · DOI · PMC13294184 |
| Ultrasound-based withdrawal of biologics in rheumatoid arthritis (RA-BioStop) | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42567558 · DOI · PMC13475499 |
| Gut Microbial Functional Ecology and Microbiota-Derived Metabolites in Rheumatoid Arthritis Autoimmunity | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 42587806 · DOI · PMC13465111 |
Immunological profiling of rheumatoid factor-positive primary Sjögren's syndrome by single-cell RNA sequencing [1]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectivePrimary Sjögren's syndrome (pSS) is a highly heterogeneous autoimmune disease.
- Closing excerpt
- RF status serves as a key stratification marker for immune heterogeneity in pSS patients, providing new insights for understanding disease mechanisms and developing targeted therapeutic strategies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (335 words)
ObjectivePrimary Sjögren's syndrome (pSS) is a highly heterogeneous autoimmune disease. Previous studies have suggested that rheumatoid factor (RF)-positive patients appear to have a higher incidence of systemic involvement. However, the underlying mechanisms remain unclear. This study aims to elucidate the potential biological mechanisms through single-cell RNA sequencing (scRNA-seq).MethodsPeripheral blood mononuclear cells from 3 healthy controls, 6 RF-negative (RF-) pSS patients, and 6 RF-positive (RF+) pSS patients were subjected to scRNA-seq. Subsequent analyses included pathway enrichment analysis, trajectory analysis, cell-cell communication analysis, and B cell receptor (BCR) and T cell receptor (TCR) repertoire profiling. Potential differences were further validated by flow cytometry.ResultsAnalysis of B cell subsets revealed a significantly increased proportion of plasma cells in RF+ patients, and differential gene expression analysis indicated enhanced pathways related to antibody production, clonal expansion, and type I interferon activation. In T-cell subsets, the RF+ group showed a notably higher proportion of CD8+ T cells, which exhibited stronger cytotoxicity and activation of interferon signaling. In contrast, mucosal-associated invariant T (MAIT) cells demonstrated activated interferon signaling but were present at a lower proportion compared to the RF- group. Cell-cell communication analysis revealed strengthened crosstalk between B cells and T cells in the RF+ group. Pseudo-time trajectory analysis further indicated that in RF+ patients, both plasma cells and CD8+ T cells exhibited a developmental skew toward a terminally differentiated state. Additionally, both BCR and TCR repertoire analyses indicated RF+ and RF- patients exhibiting distinct patterns in clonal distribution and frequency. Flow cytometry further validated the increased proportion of CD8+ T cells and the decreased proportion of MAIT cells in the peripheral blood of RF+ pSS patients.ConclusionThe RF status in pSS patients is closely associated with specific immune cell profiles. RF+ patients exhibit more active plasma cell responses, enhanced CD8+ T-cell cytotoxicity and interferon responses, as well as heightened interferon signaling yet reduced proportion of MAIT cells. RF status serves as a key stratification marker for immune heterogeneity in pSS patients, providing new insights for understanding disease mechanisms and developing targeted therapeutic strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42367820 · DOI · PMC13294184
Ultrasound-based withdrawal of biologics in rheumatoid arthritis (RA-BioStop) [2]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectiveTo test whether ultrasonography of patients with rheumatoid arthritis (RA) in the American College of Rheumatology/the European Alliance of Associations for Rheumatology (ACR/EULAR) remission is useful for prediction of relapse after discontinuation of a biological disease-modifying antirheumatic drug (bDMARD).
- Closing excerpt
- Trial registration numberNCT01602302.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (256 words)
ObjectiveTo test whether ultrasonography of patients with rheumatoid arthritis (RA) in the American College of Rheumatology/the European Alliance of Associations for Rheumatology (ACR/EULAR) remission is useful for prediction of relapse after discontinuation of a biological disease-modifying antirheumatic drug (bDMARD).MethodsProspective trial including patients with RA in persistent ACR/EULAR remission treated with conventional synthetic DMARDs plus bDMARDs. After stopping the bDMARD, nine study visits including clinical examination and ultrasound of 14 joints (blinded to clinical data) were conducted within 52 weeks. The primary hypothesis was that a Power Doppler (PD) score≥1 predicted relapse occurring within week 16 after bDMARD cessation. Relapse was defined as a change from remission to moderate/high disease activity according to the Simplified Disease Activity Score.ResultsInclusion of 110 patients was originally planned; however, the study was terminated after reaching 38 (34.5%) patients due to insufficient recruitment. Relapses till week 16 were numerically more common in patients with PD score≥1 at baseline than in those with PD=0 (9/30 (30.0%) vs 0/7 (0%), p=0.160). Similar observations were made for weeks 24 and 52. PD scores were higher at the time of relapse than at preceding visits (mean PD score difference: 3.2 (±4.5) points, p=0.034). There were trends towards a higher baseline PD score in patients who had a relapse until week 16 as compared with those who remained in remission (5.2±5.8 vs 2.3±3.0, p=0.079).ConclusionThe primary endpoint was not reached. The presented data should be interpreted as hypothesis-generating, serving to stimulate future research on the value of ultrasound in assessing remission and predicting relapse in RA.Trial registration numberNCT01602302.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42567558 · DOI · PMC13475499
Gut Microbial Functional Ecology and Microbiota-Derived Metabolites in Rheumatoid Arthritis Autoimmunity [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The gut microbiota is a key regulatory hub linking environmental exposure, the mucosal barrier, and joint inflammation, and plays an important role in the pathogenesis and progression of rheumatoid arthritis (RA).
- Closing excerpt
- This review aims to shift RA microbiome research from taxonomic profiling toward stage-specific functional ecological analysis, providing a basis for risk stratification, therapeutic response prediction, and microbiota-based adjunctive interventions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (216 words)
The gut microbiota is a key regulatory hub linking environmental exposure, the mucosal barrier, and joint inflammation, and plays an important role in the pathogenesis and progression of rheumatoid arthritis (RA). Mechanistic studies in this field mainly address two interrelated questions: how RA-associated gut microbiota modulate mucosal immunity and systemic autoimmunity through strain-level variation, niche competition, and metabolic remodeling; and how disease stage, host immune status, and drug exposure reciprocally reshape gut microbial structure and function. Accordingly, this review follows the framework of "anti-inflammatory/pro-inflammatory microbial niches-microbiota-derived metabolites-immune cell homing and migration" to summarize recent advances in the role of gut microbiota and their derivatives in RA onset, progression, and therapeutic response. Focusing on disease-stage-specific remodeling of gut functional ecology, we discuss how short-chain fatty acids, tryptophan-derived indoles, bile acids, succinate, and other microbial effector molecules regulate RA immunopathology through regulatory T cells (Treg), regulatory B cells (Breg), type 17 T helper cells (Th17), and IL-17-producing T follicular helper cells (Tfh17), dendritic cells, fibroblast-like synoviocytes, and osteoclasts. We also highlight intestinal antigen sampling, autoantibody generation, immune cell trafficking, and synovial reactivation as key links in the gut-joint axis. This review aims to shift RA microbiome research from taxonomic profiling toward stage-specific functional ecological analysis, providing a basis for risk stratification, therapeutic response prediction, and microbiota-based adjunctive interventions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42587806 · DOI · PMC13465111
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Multi-ancestry genome-wide association analyses identify novel genetic mechanisms in rheumatoid arthritis [4]
- Research article Prevalence, imaging patterns and risk factors of interstitial lung disease in connective tissue disease: a systematic review and meta-analysis [5]
- Research article Gut dysbiosis in rheumatic diseases: A systematic review and meta-analysis of 92 observational studies [6]
- Research article Efficacy and Safety of Curcumin and Curcuma longa Extract in the Treatment of Arthritis: A Systematic Review and Meta-Analysis of Randomized Controlled Trial [7]
- Research article Effect of Anti-Inflammatory Diets on Pain in Rheumatoid Arthritis: A Systematic Review and Meta-Analysis [8]
- Research article Telemedicine application in patients with chronic disease: a systematic review and meta-analysis [9]
References
- Wang Y, Ji W, Teng F, Han Y, Xu H, Zhi Y, et al.. Immunological profiling of rheumatoid factor-positive primary Sjögren's syndrome by single-cell RNA sequencing. . 2026. PMID 42367820 · DOI · PMC13294184
- Dejaco C, Gessl I, Husic R, Mitter G, Deimel T, Lackner A, et al.. Ultrasound-based withdrawal of biologics in rheumatoid arthritis (RA-BioStop). . 2026. PMID 42567558 · DOI · PMC13475499
- Rong X, Zhang X, Tan Y, Lu C. Gut Microbial Functional Ecology and Microbiota-Derived Metabolites in Rheumatoid Arthritis Autoimmunity. . 2026. PMID 42587806 · DOI · PMC13465111
- Ishigaki K, Sakaue S, Terao C, Luo Y, Sonehara K, Yamaguchi K, et al.. Multi-ancestry genome-wide association analyses identify novel genetic mechanisms in rheumatoid arthritis. Nat Genet. 2022. PMID 36333501 · DOI · PMC10165422
- Joy GM, Arbiv OA, Wong CK, Lok SD, Adderley NA, Dobosz KM, et al.. Prevalence, imaging patterns and risk factors of interstitial lung disease in connective tissue disease: a systematic review and meta-analysis. Eur Respir Rev. 2023. PMID 36889782 · DOI · PMC10032591
- Wang Y, Wei J, Zhang W, Doherty M, Zhang Y, Xie H, et al.. Gut dysbiosis in rheumatic diseases: A systematic review and meta-analysis of 92 observational studies. EBioMedicine. 2022. PMID 35594658 · DOI · PMC9120231
- Zeng L, Yang T, Yang K, Yu G, Li J, Xiang W, et al.. Efficacy and Safety of Curcumin and Curcuma longa Extract in the Treatment of Arthritis: A Systematic Review and Meta-Analysis of Randomized Controlled Trial. Front Immunol. 2022. PMID 35935936 · DOI · PMC9353077
- Schönenberger KA, Schüpfer AC, Gloy VL, Hasler P, Stanga Z, Kaegi-Braun N, et al.. Effect of Anti-Inflammatory Diets on Pain in Rheumatoid Arthritis: A Systematic Review and Meta-Analysis. Nutrients. 2021. PMID 34959772 · DOI · PMC8706441
- Ma Y, Zhao C, Zhao Y, Lu J, Jiang H, Cao Y, et al.. Telemedicine application in patients with chronic disease: a systematic review and meta-analysis. BMC Med Inform Decis Mak. 2022. PMID 35440082 · DOI · PMC9017076
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.