Autoimmunity, infectious immunity, and atherosclerosis

Authors: Matsuura E (1) , Kobayashi K (1) , Matsunami Y (1) , Shen L (1,2) , Quan N (1,3) , Makarova M (1,4) , Suchkov SV (4) , Ayada K (2) , Oguma K (2) , Lopez LR (5)

Affiliations:

(1) Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences (2) Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences (3) Cardiovascular Center, The First Hospital of Jilin University (4) Department of Pathology, I.M. Sechenov Moscow Medical Academy (5) Corgenix Inc.

Source: J Clin Immunol. 2009 Nov;29(6):714-21

DOI: 10.1007/s10875-009-9333-5 Publication date: 2009 Nov E-Publication date: Oct. 1, 2009 Availability: abstract Copyright: Not specified

Language: English Countries: Not specified Location: Not specified Correspondence address: eijimatu@md.okayama-u.ac.jp

Keywords

Article abstract

INTRODUCTION:

Vascular inflammation is common in certain systemic autoimmune diseases and contributes to the oxidation of low-density lipoprotein (oxLDL) and oxLDL/beta2-glycoprotein I (beta2GPI) 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/beta2GPI complexes increases in the presence of IgG anti-beta2GPI antibodies and that IgG immune complexes containing oxLDL/beta2GPI upregulate the expression of both scavenger and Fcgamma receptors to activate beta2GPI 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) maybe protective. We review the recent progress in our understanding of autoimmunity and infectious immunity that promote atherosclerosis.

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