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.
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.
Authors: P Saikku; M Leinonen; K Mattila; M R Ekman; M S Nieminen; P H Mäkelä; J K Huttunen; V Valtonen Journal: Lancet Date: 1988-10-29 Impact factor: 79.321
Authors: T Inaba; M Mizuno; S Take; K Suwaki; T Honda; K Kawai; M Fujita; T Tamura; K Yokota; K Oguma; H Okada; Y Shiratori Journal: Eur J Clin Invest Date: 2005-03 Impact factor: 4.686
Authors: L Erkkilä; K Laitinen; K Haasio; T Tiirola; M Jauhiainen; H A Lehr; K Aalto-Setälä; P Saikku; M Leinonen Journal: Atherosclerosis Date: 2004-12 Impact factor: 5.162
Authors: K Yokota; Y Hirai; M Haque; S Hayashi; H Isogai; T Sugiyama; E Nagamachi; Y Tsukada; N Fujii; K Oguma Journal: Microbiol Immunol Date: 1994 Impact factor: 1.955
Authors: Rohina Rubicz; Charles T Leach; Ellen Kraig; Nikhil V Dhurandhar; Barry Grubbs; John Blangero; Robert Yolken; Harald Hh Göring Journal: BMC Res Notes Date: 2011-10-21
Authors: Margit Keresztes; Tamás Horváth; Imre Ocsovszki; Imre Földesi; Gyöngyi Serfőző; Krisztina Boda; Imre Ungi Journal: PLoS One Date: 2013-08-14 Impact factor: 3.240