Abstract
The sequestering of oxidation-modified low-density lipoprotein by macrophages results in the accumulation of fatty deposits within the walls of arteries. Necrosis of these cells causes a release of intercellular epitopes and the activation of the adaptive immune system, which we predict leads to robust autoantibody production. T cells produce cytokines that act in the plaque environment and further stimulate B cell antibody production. B cells in atherosclerosis meanwhile have a mixed role based on subclass. The current model is that B-1 cells produce protective IgM antibodies in response to oxidation-specific epitopes that work to control plaque formation, while follicular B-2 cells produce class-switched antibodies (IgG, IgA, and IgE) which exacerbate the disease. Over the course of this review, we discuss further the validation of these protective antibodies while evaluating the current dogma regarding class-switched antibodies in atherosclerosis. There are several contradictory findings regarding the involvement of class-switched antibodies in the disease. We hypothesize that this is due to antigen-specificity, and not simply isotype, being important, and that a closer evaluation of these antibodies' targets should be conducted. We propose that specific antibodies may have therapeutical potential in preventing and controlling plaque development within a clinical setting.