B cells interactions in lipid immune responses: implications in atherosclerotic disease

Abstract

Atherosclerosis is considered as an inflammatory and chronic disorder with an important immunologic component, which underlies the majority of cardiovascular diseases; condition that belongs to a group of noncommunicable diseases that to date and despite of prevention and treatment approaches, they remain as the main cause of death worldwide, with 17.5 million of deaths every year. The impact of lipids in human health and disease is taking center stage in research, due to lipotoxicity explained by elevated concentration of circulating lipids, in addition to altered adipose tissue metabolism, and aberrant intracellular signaling. Immune response and metabolic regulation are highly integrated systems and the proper function of each one is dependent on the other. B lymphocytes express a variety of receptors that can recognize foreign, endogenous or modified self-antigens, among them oxidized low density lipoproteins, which are the main antigens in atherosclerosis. Mechanisms of B cells to recognize, remove and present lipids are not completely clear. However, it has been reported that B cell can recognize/remove lipids through a range of receptors, such as LDLR, CD1d, FcR and SR, which might have an atheroprotector or proatherogenic role during the course of atherosclerotic disease. Pertinent literature related to these receptors was examined to inform the present conclusions.

Keywords: Atherosclerosis; B cells; CD1 receptors; Cardiovascular diseases; Fc receptors; Lipids; Scavenger receptors.

Fig. 1

Participation of B cell receptors during atherosclerotic plaque formation. During atherosclerotic plaque formation we speculate that B cells have an important participation. The expression of LDLR contributes with the recognition of LDL molecules and its antigenic presentation trough CD1d to iNKTs exacerbates the disease. Persistence presence of LDL molecule favors its oxidation; oxLDLs are recognized by CD36 and SR-BI, leading to the development of lipid load cells either contributing to atherosclerosis (panel in red) or depending on the disease stage, diminishing the inflammatory process (panel in green). On the contrary, the up regulation of FcγRIIB receptors with inhibitory activity induce anti-inflammatory responses after recognition of immune complexes of IgG and oxLDL associated with an atheroprotector role (panel in green)