Adaptive immunity-driven inflammation and cardiovascular disease

Abstract

The adaptive immune response has recently emerged as an important factor in a wide variety of cardiovascular disorders including atherosclerosis, hypertension, cardiac remodeling, and heart failure; however, its role is not fully understood. Since an assortment of innate responsive cells, e.g., neutrophils and monocytes/macrophages, coordinate with adaptive immunity, e.g., T cells, dendritic cells, and B cells, the temporal response and descriptions pertinent to the cellular phenotype and inflammation processes, in general, need additional investigation, clarification, and consensus particularly in cardiovascular disease. This Perspectives article reviews the contributions of 15 articles (including 7 reviews) published in the American Journal of Physiology-Heart and Circulatory Physiology in response to the Call for Papers: Adaptive Immunity in Cardiovascular Disease. Here, we summarize the crucial reported findings at the cardiac, vascular, immune, and molecular levels and discuss the translational feasibility and benefits of future prospective research into the adaptive immune response. Readers are encouraged to evaluate the data and learn from this collection of novel studies.

Targets of Vitamin C With Therapeutic Potential for Cardiovascular Disease and Underlying Mechanisms: A Study of Network Pharmacology

“…Oxidative stress and inflammation play a crucial role in the onset and progression of atherosclerosis and the development of cardiovascular events ( Pignatelli et al, 2018 ; Ilatovskaya et al, 2019 ). Inflammation promotes oxidative stress, which in turn leads to further inflammation, therefore establishing a self-perpetuating cycle.…”

<p>Reflections on Atherosclerosis: Lesson from the Past and Future Research Directions</p>

“…T cells are among the first cells to be recruited into atherosclerotic lesion. [79][80][81][82] The adaptive response is based on CD4 + and CD8 + T cells activation and antibody secretion by B cells. Once activated, CD4+ T cells multiply and differentiate into specialized effector T helper (Th) lymphocytes, while activated CD8+ T cells multiply and differentiate into cytotoxic CD8+ T lymphocytes.…”

“…Th17 cells produce IL-17 which has different effects on lesions, emphasizing endothelial inflammation but also increasing fibrosis and promoting plaque stability. [79][80][81][82] Treg cells are immunoregulatory cells with atheroprotective properties: they secrete the immunosuppressive cytokines such as transforming growth factor-beta (TGF-β), IL-10 and IL-35, which exert anti-inflammatory actions. 83…”

Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents

“…Oxidative stress has been shown to activate hypertrophic and pro-inflammatory pathways and thus could be, in part, responsible for cardiac hypertrophy and higher collagen deposition, as previously mentioned [ 89 ]. Indeed, inflammation and immune cells are crucial in the initiation, development, and progression to chronicity of several cardiovascular diseases, such as hypertension [ 90 ], atherosclerosis [ 91 ] or pathologies affecting cardiac injury and repair [ 92 ] and involve the innate and adaptive immune responses [ 93 , 94 ]. Again, these biochemical changes associated with higher inflammatory status and oxidative stress might be involved in the alterations of cardiac contractile function and predispose the heart to a higher sensitivity to ischemic or toxic injuries.…”