Gene expression profiling of immune cells in blood from patients with coronary Artery Disease 2235454
Abstract 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. Funding Source n/a Topic Categories Immune Mechanisms of Human Disease (HUM)
Authors
- Michael Nakama
- A. Bellapu (ORCID: https://orcid.org/0000-0003-0605-1063)
- Payel Roy (ORCID: https://orcid.org/0000-0003-2511-068X)
- Klaus Ley (ORCID: https://orcid.org/0000-0003-1124-9592)
- Aderonke Fakayode
- Ruibo Cai
- Austin W T Chiang
- Martina Zocchedu
Institutions
- Augusta University Health (US)
- Indian Institute of Science Bangalore (IN)
Publication Details
- Journal
- The Journal of Immunology
- Published
- 2026-07-28
- DOI
- https://doi.org/10.1093/jimmun/vkag141.028
- Primary Topic
- Atherosclerosis and Cardiovascular Diseases
- Type
- article
- Field-Weighted Citation Impact
- 0.00