Abstract
Cardiovascular diseases (CVD) include a wide range of disorders affecting the heart and blood vessels, many of which are associated with atherosclerosis. Atherosclerosis is the main underlying cause of CVDs and represents a chronic inflammatory disease of the large arteries involving the build-up of plaques within the arterial wall. B cells play a dual role in CVD, particularly in the context of atherosclerosis, by producing antibodies and secreting cytokines that modulate inflammation. Depending on their subtype (B1 vs. B2 cells) and the specific context, B cells can have both protective and harmful effects on the cardiovascular system. B1 cells, which arise predominantly during fetal development, are found in body cavities, such as the perivascular adipose tissue (PVAT) and peritoneum. Guided by CXCL13 and CCR6, they migrate to sites, where they produce IgM and IgG3, contributing to immune regulation and pathogen defense. In contrast, B2 cells-central players in adaptive immunity-originate in the bone marrow and mature in secondary lymphoid organs. Within this subset, marginal-zone (MZ) B cells provide rapid, low-affinity IgM responses to blood-borne antigens, while follicular (FO) B cells mediate high-affinity, T-cell-dependent antibody production. For all of the latter chemokine-guided migration is essential for B-cell function, from immune surveillance to antibody secretion. Receptors such as CXCR4, CXCR5, and ACKR3 not only direct B-cell trafficking but also influence their phenotype in cardiovascular disease. Understanding how these chemokine-receptor interactions shape B-cell-mediated immunity in CVD may allow for developing targeted therapies for atherosclerosis, myocardial infarction, and stroke.