Key result
Multi-omics profiling in CAD reveals distinct immune states and oligoclonal expansion of ApoB-reactive T cells.
Why the study?
Coronary artery disease is increasingly recognized as an immune-mediated disorder, and defining immune alterations can provide mechanistic insights and therapeutic targets.
Cross-Sectional (n=39)
Single-cell multi-omics reveals antigen-driven T-cell responses to ApoB epitopes in CAD patients, highlighting potential targets for precision immunotherapy.
Answers are grounded in this paper and cite their sources.
Peripheral immune profiling in CAD offers mechanistic insights; leaves open therapeutic targeting pending larger validation studies.
Introduction Coronary artery disease (CAD) is a leading cause of death worldwide and is increasingly recognized as an immune-mediated disorder. Defining immune alterations in CAD can provide mechanistic insights and therapeutic targets. Methods Single-cell multi-omics (RNA- and CITE-seq) was applied to profile peripheral blood mononuclear cells from 39 CAD patients undergoing coronary angiography. After quality control and integration (∼416,000 singlet cells), we analyzed major immune lineages, transcriptional and proteomic states, and T-cell receptor repertoires. Results Distinct states of T cells, B cells, NK cells, and monocytes were identified. Weighted nearest neighbor analysis revealed subsets with altered activation and checkpoint signatures, including heterogeneous CD4+ T-cell populations. TCR sequencing demonstrated oligoclonal expansion of 335 clones by TCRB CDR3 sequences. GLIPH2 clustering revealed enrichment of MHC-II—restricted motifs with reactivity to ApoB epitopes, highlighting antigen-driven T-cell responses as potential contributors to CAD progression and potential targets for precision immunotherapy Conclusion Integrating this new dataset with published datasets provides an integrated atlas of immune dysregulation in CAD.
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Fakayode et al. (2026) conducted a cross-sectional in Coronary artery disease (n=39). Coronary artery disease was evaluated on Immune cell transcriptional and proteomic states and T-cell receptor repertoires.
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