Autoimmunity, infectious immunity, and atherosclerosis

Introduction: Vascular inflammation is common in certain systemic autoimmune diseases and contributes to the oxidation of low-density lipoprotein (oxLDL) and oxLDL/β2-glycoprotein I (β2GPI) complex formation. These complexes have been implicated as proatherogenic autoantigens that participate in the development of atherosclerotic disease. Discussion: We have demonstrated that the in vitro macrophage uptake of oxLDL/β2GPI complexes increases in the presence of IgG anti-β2GPI antibodies and that IgG immune complexes containing oxLDL/β2GPI upregulate the expression of both scavenger and Fcγ receptors to activate β2GPI-specific T cells. Some persistent infections may cause immune responses that promote atherogenesis. Cellular immunity (Th1) against Helicobacter pylori (H. pylori) derived heat shock protein 60 (Hp-HSP60) cross-reacts with endogenous HSP60 to cause cardiovascular disease likely by molecular mimicry. Conclusion: Infectious cellular response may be proatherogenic, while the humoral response (antibody production) may be protective. We review the recent progress in our understanding of autoimmunity and infectious immunity that promote atherosclerosis.