Editorial: The Interplay Between Immune Activation and Cardiovascular Disease During Infection, Autoimmunity and Aging: The Role of T Cells

Chronic activation of cells of the immune system including T cells and systemic inflammation are well known risk factors for cardiovascular disease (CVD). Many human pathological conditions including viral infections, autoimmune diseases and aging are recognized drivers of increased risk of CVD. Among viral infections, Cytomegalovirus (CMV) infection is a contributing risk element to the existing traditional risk factors of atherogenesis; Influenza infection is correlated with ncreased the risk of cardiovascular events leading to deaths and HIV infection is an independent predictor of cardiovascular risk. The pandemic of SARS-COV2 infection showed that the severe presentation of the disease manifests with vascular damage and cardiovascular events. Autoimmune and chronic inflammatory diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and psoriatic disease are also associated with cardiovascular disease. Lastly, in adults over 65 years, the accumulation of age-related phenotypic and functional alterations in immune cells parallels with a decline of the cardiovascular system with an increased incidence of cardiovascular disease. The mechanisms behind are not well defined, and while the role of innate immune cells has been established, the involvement of T cells in promoting vascular pathology and cardiovascular disease has emerged more recently (1). Chronic systemic inflammation and increased circulating levels of cytokines and chemokines can indeed contribute to vascular damage by promoting endothelial cell activation and oxidative stress thus linking to the increased risk of CVD (2, 3). Activation of endothelial cells promotes recruitment of circulating immune cells including T cells that will be activated and differentiate into distinct effector cells contributing to the pathology of the disease (4–6). Endothelial cells in this context have also been proposed to act as “semiprofessional” antigen presenting cells (APC) presenting antigens and providing several costimulatory signals to T cells leading to T cell activation especially at sites defined as endothelium-dependent microvascular reactivity sites by Laser Doppler Flowmetry Assessment (7). A milestone in the understanding the role of T cells in promoting vascular inflammation has been reached with the characterization of the immune cell infiltrate in human atherosclerotic plaque by scRNA-seq technology which defined the main subsets of T cells in atherosclerosis (8). This data paved the way for further investigations about the role of T cells as a putative mechanistic link in pathologies associated with an increased risk of CVD. The proposed mechanisms by which T cells contribute to the pathology of the disease include dysregulated T helper and CD8 T cell function, expansion of terminally differentiated cytotoxic effectors CD4+ CD28- T cells and impaired Tregs function. This Research Topic has the aim to provide an overview of the latest advances in the study of the role of T cell activation and endothelial inflammation in cardiovascular risk and disease in the context of infection, autoimmunity and aging. The Research Topic highlights the emerging common and distinctive features of the putative immune mechanistic links between the pathophysiological conditions and the associated cardiovascular disease. The Research Topic comprises 11 articles, original research articles, 5 review and one systematic review and was divided into 3 sections. 1. Endothelial inflammation and T cell activation in CVD associated with infection. 2. T cell mechanisms involved in CVD associated with autoimmune diseases. 3. The immunology of cardiovascular disease during aging.