The process of antigen presentation bridges innate and adaptive immunity, which plays a crucial role in shaping inflammation across a wide range of cardiovascular diseases, including atherosclerosis. Professional antigen-presenting cells, such as dendritic cells, macrophages, and B cells, accumulate within the arterial wall, giving them the potential to present self-derived antigens via major histocompatibility complex (MHC) molecules. This process drives the activation and differentiation of T cells through both MHC class II–restricted CD4⁺ T-cell responses and MHC class I–restricted CD8⁺ T-cell. However, compared with other chronic inflammatory diseases, the mechanisms regulating antigen presentation, cross-presentation, and immune cell cross-talk within cardiovascular tissues remain incompletely defined. Understanding how antigen presentation shapes immune responses in the vasculature and heart is critical for identifying new immunomodulatory strategies to promote plaque stability and prevent cardiovascular events.
Despite growing evidence that antigen presentation critically shapes immune responses in cardiovascular diseases, the mechanisms governing this process within vascular tissues and the heart remain poorly defined. It is still unclear which antigen-presenting cells predominate across disease stages, how self- and modified self-antigens are processed and presented, and how antigen presentation drives pathogenic versus protective T-cell responses. In particular, the contributions of MHC class I–restricted antigen presentation and cross-presentation to CD8⁺ T-cell activation in atherosclerotic plaques remain poorly understood. Addressing this gap requires integrating advanced cellular and molecular immunological approaches. Recent advances, including single-cell and spatial transcriptomics, high-dimensional flow cytometry, and antigen-specific T-cell tracking models, now enable precise mapping of antigen-presenting cell–T-cell interactions within the arterial wall and heart. Leveraging these technologies will enable the field to define context-specific antigen presentation pathways and identify immunomodulatory strategies that selectively dampen cardiovascular inflammation while preserving systemic immune competence.
This Research topic aims to advance understanding of how antigen presentation shapes immune responses in cardiovascular diseases, with a particular focus on atherosclerosis and related inflammatory vascular disorders as well as myocardial diseases. We welcome contributions addressing, but not limited to, the following themes:
• Antigen-presenting cell subsets in cardiovascular tissues, including dendritic cells, macrophages, B cells, and non-classical antigen-presenting cells. • Mechanisms of MHC class I and class II antigen presentation and cross-presentation in the arterial wall and heart tissue. • Antigen-specific CD4⁺ and CD8⁺ T-cell responses in plaque development, progression, and stability • Immune cell cross-talk linking antigen presentation to innate immune regulation. • Spatial, temporal, and metabolic regulation of antigen presentation in cardiovascular disease. • Therapeutic strategies targeting antigen presentation pathways to modulate cardiovascular inflammation.
We welcome reviews, mini-reviews, and perspectives employing experimental and translational, approaches.
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Article types
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
Case Report
Classification
Clinical Trial
Editorial
FAIR² Data
FAIR² DATA Direct Submission
General Commentary
Hypothesis and Theory
Methods
Mini Review
Opinion
Original Research
Perspective
Review
Systematic Review
Technology and Code
Keywords: Cardiovascular diseases, antigen presentation, MHC-I, MHC-II, dendritic cells, macrophages, B cells, CD4, CD8, T Cells
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