Cardiovascular disease (CVD) causes nearly half of all deaths in Europe (48%), costing a dramatic €196 billion a year. Despite the reduction in mortality that has been achieved over the past decades, 70% of cardiovascular (CV) events cannot be prevented with the treatment of known risk factors. Aggressive glucose metabolism control in Type 2 Diabetes did not automatically result in CVD prevention and lipid-lowering agents beyond statins have not yet delivered the expected reduction in CV events highlighting a complex relationship between inflammation and hyperlipidaemia.
The treatment of risk factors, albeit beneficial, has reached its full potential in CVD and new treatments should be targeted to novel disease factors.
Inflammation is the important component of the pathogenesis of CVD that is not yet therapeutically targeted.
B cells are a classic example of the contrasting role of immune cell subsets in CVD.
Recent studies demonstrated that B cells carry out both pro- and anti-atherogenic functions and that these dual roles are executed by different B cell subsets in CVD. Thus, as in many other immune disorders, B cells contribute to both CVD pathogenesis as well as to protection from CVD.
The limited knowledge of B cell function in atherosclerosis is hampering the discovery of therapeutic opportunities in CVD and current therapies targeting B cells are limited to antibodies for B cell depletion that do not discriminate the B cell subsets and are associated with risks of immunosuppression.
The outstanding question is which B cell subsets confer protection versus pathogenicity and which mechanisms do B cell subtypes use to do this.
Harnessing protective or abating unwanted B cell responses has the potential to shed light on the pathogenesis of CVD, increase our knowledge of pathogenic versus protective B cell responses in CVD and thus permit the identification and validation of unexplored therapeutic targets for the prevention and treatment of atherosclerosis.