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Association of Elevations of Specific T Cell and Monocyte Subpopulations in Rheumatoid Arthritis With Subclinical
Robert Winchester1, Jon T Giles1, Simona Nativ1
1Columbia University College of Physicians and Surgeons, New York, New York.
Insights
Certain peripheral blood mononuclear cell (PBMC) subsets are linked to coronary artery calcification (CAC) in rheumatoid arthritis (RA) patients. These findings may indicate shared pathways in RA and cardiovascular disease.
Area of Science:
- Immunology
- Cardiology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) significantly increases the risk of coronary artery disease (CAD), the leading cause of mortality in RA patients.
- Identifying specific biomarkers for CAD risk in RA is crucial for early intervention.
- Alterations in peripheral blood mononuclear cell (PBMC) subsets, including T cell activation and inflammatory monocytes, are observed in RA patients.
Purpose of the Study:
- To investigate whether elevated PBMC subpopulations in RA patients are associated with subclinical CAD, assessed by coronary artery calcification (CAC).
Main Methods:
- Seventy-two RA patients underwent cardiac computed tomography for CAC assessment.
- PBMC subsets were analyzed using multiparameter flow cytometry.
- Multivariable logistic regression models were employed to determine associations between PBMC subsets and CAC presence.
Main Results:
- 33% of RA patients had detectable CAC.
- Patients with CAC showed significantly higher levels of activated CD4 T cell subsets and CD8 T cell subsets with effector memory phenotypes.
- Elevated CD14(high)CD16+ intermediate monocytes were also observed in patients with CAC.
- Increased CD4+CD56+CD57+ T cells and CD14(high)CD16+ monocytes remained independently associated with CAC after multivariable adjustment.
Conclusions:
- Specific PBMC subsets serve as potential biomarkers for the presence of CAC in RA patients.
- These findings suggest that PBMC alterations may contribute to atherogenesis in RA, potentially through shared etiologic pathways with cardiovascular disease.
Objective:
Coronary artery disease (CAD) is the leading cause of excess deaths in rheumatoid arthritis (RA). However, identification of features denoting patients with a risk of developing CAD is lacking. The composition of circulating peripheral blood mononuclear cell (PBMC) subsets in RA patients differs markedly from that in healthy controls with regard to the extent of T cell activation, with clonal expansion and differentiation to effector memory status, and presence of inflammatory monocytes. In this study, we sought to evaluate whether elevations in these PBMC subpopulations in RA patients could denote those with an increased risk of subclinical CAD, as determined by the presence of coronary artery calcification (CAC).
Methods:
The study cohort comprised 72 patients with RA who underwent cardiac computed tomography to assess CAC. PBMC subsets were determined by multiparameter flow cytometry. Multivariable logistic regression was used to determine the associations between PBMC subpopulations and the presence of CAC.
Results:
Among the 72 patients with RA, 33% had CAC and exhibited significant increases in the levels of circulating CD4 T cell subsets denoting activation and differentiation to the effector memory phenotypes. Analogous increases in the levels of CD8 T cell subsets, as well as in the CD14(high)CD16+ intermediate monocyte subset, were also present in these patients, as compared to those without CAC. The increases in the CD4 and CD8 T cell subsets were highly intercorrelated, whereas the increases in CD14(high)CD16+ monocytes were independent of elevations in the CD4 T cell subsets. After adjustments for relevant confounders, the levels of CD4+CD56+CD57+ T cells and CD14(high)CD16+ monocytes remained associated with the presence of CAC.
Conclusion:
These findings indicate that PBMC subsets are markers for the presence of CAC and suggest that mechanisms of atherogenesis in RA may operate in part through the elevations in these subsets, raising further questions about the mechanisms underlying the presence of such alterations in cell composition in patients with RA and the potential for shared etiologic pathways between RA and cardiovascular disease.
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