Autoimmunity, Infectious Immunity, and Atherosclerosis

作者：Matsuura Eiji^*; Kobayashi Kazuko; Matsunami Yukana; Shen Lianhua; Quan Nanhu; Makarova Marina; Suchkov Sergey V; Ayada Kiyoshi; Oguma Keiji; Lopez Luis R

来源：Journal of Clinical Immunology, 2009, 29(6): 714-721.

DOI：10.1007/s10875-009-9333-5

• Atherosclerosis
• autoimmunity
• infection
• beta 2-glycoprotein I (beta 2GPI)
• heat shock protein 60 (HSP60)

Vascular inflammation is common in certain systemic autoimmune diseases and contributes to the oxidation of low-density lipoprotein (oxLDL) and oxLDL/beta 2-glycoprotein I (beta 2GPI) complex formation. These complexes have been implicated as proatherogenic autoantigens that participate in the development of atherosclerotic disease.
We have demonstrated that the in vitro macrophage uptake of oxLDL/beta 2GPI complexes increases in the presence of IgG anti-beta 2GPI antibodies and that IgG immune complexes containing oxLDL/beta 2GPI upregulate the expression of both scavenger and Fc gamma receptors to activate beta 2GPI-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.
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.

• 出版日期2009-11
• 单位吉林大学