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Associations of Immune Cell Subsets With Coronary Artery Calcium Incidence and Progression in the Multi‐Ethnic Study of Atherosclerosis

Year: 2025
Type: article
Abstract: Background Limited data exist on associations of immune cell subsets with longitudinal changes in subclinical coronary artery disease. Methods In the MESA (Multi‐Ethnic Study of Atherosclerosis) study, we used a case‐cohort approach to explore associations of 28 immune cell subsets measured at baseline (2000–2002) with longitudinal changes in coronary artery calcium ( CAC ). We examined incident CAC from examination 2 (2002–2004) through examination 5 (2010–2012) in participants with 0 CAC at baseline using multivariable‐adjusted Cox regression. In participants with CAC >0 at baseline, we analyzed changes in CAC through examination 5 using multivariable‐adjusted linear mixed models. Because no studies have investigated immune cells and longitudinal CAC changes, analyses were considered exploratory, with P <0.05 as the threshold for possible significance. Results Of 975 participants with immune cells subsets and CAC measurements at baseline, 378 had CAC 0 at baseline (mean age, 58.4; 37.0% men) and 597 had CAC >0 at baseline (mean age, 65.7; 57.6% men). Natural killer cells were associated with higher incident CAC (hazard ratio [ HR], 1.26 per SD higher natural killer cell proportion; P =0.03), whereas T helper type cells were associated with lower incident CAC ( HR , 0.81; P =0.04). B cells were associated with CAC progression (β=53.1 Agatston units per SD higher B‐cell proportion, P =0.04), whereas CD14 + CD16 + monocytes (β=−71.6; P =0.03) and T regulatory cells (β=−61.9; P =0.03) were associated with lower CAC progression. Conclusions Natural killer cells may be associated with incident CAC and T regulatory cells may be associated with attenuated CAC progression, among other findings. These warrant replication and experimental investigation.
Language: English
Subfield: Immunology
Open Access status: gold
Estimated APC paid: $3,810
OpenAlex ID: W4414354442
FWCI: 0.883
Cites: 26
Cited by: 3
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