ArticleClinical rheumatology2026
Association of Th17/Treg immune imbalance and cardiovascular complications in RA patients: retrospective cohort study in refractory subgroups.
Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
- Pathogenic Drivers of Difficult-to-Treat Rheumatoid Arthritis: Synovium and Beyond.International journal of molecular sciences · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundPatients with rheumatoid arthritis (RA) face significantly elevated cardiovascular risks, yet the underlying immunological mechanisms remain incompletely understood, particularly in refractory RA subgroups.
objectiveTo investigate the association between Th17/Treg immune imbalance and cardiovascular complications in RA patients, with a focus on delineating the unique pathological mechanisms in refractory subgroups.
methodsThis single-center retrospective cohort study (2015-2024) included 3,464 RA patients (1,872 common RA; 1,592 refractory RA) diagnosed per 2010 ACR/EULAR criteria. Flow cytometry quantified Th17 and Treg absolute counts and ratios. Patients were stratified into four immunophenotypic subgroups: Group A (Treg-deficient/Th17-normal-or-low), Group B (Treg-normal-or-high/Th17-normal-or-low), Group C (Treg-normal-or-high/Th17-high), and Group D (Treg-deficient/Th17-high). Cardiovascular outcomes included coronary artery disease, myocardial infarction, and related events.
resultsIn all RA, elevated Th17/Treg ratios correlated with increased cardiovascular risk (χ
conclusionTh17/Treg imbalance serves as a central predictor of cardiovascular risk in general RA, whereas Treg deficiency dominates in refractory RA. The interplay between immune dysregulation (Treg exhaustion), pro-inflammatory HDL remodeling, and behavioral factors constructs an "immune-metabolic-environmental" axis driving cardiovascular pathogenesis. These findings provide novel biomarkers and precision intervention targets for stratified RA management. Key Points • Treg absolute count, not Th17/Treg ratio, independently predicts cardiovascular events in refractory RA. • A novel immunophenotypic stratification (Groups A-D) identifies high-risk Group A with the highest CAD incidence. • Treg deficiency drives pro-inflammatory HDL remodeling, revealing an immune-metabolic crosstalk in RA. • Distinct mechanisms exist between common and refractory RA, defining an integrated immune-metabolic-environmental axis.
Indexed as
Identifiers
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Registered trials
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