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BMC Medicine

, 11:117

First Online: 01 May 2013Received: 21 January 2013Accepted: 15 April 2013DOI: 10.1186-1741-7015-11-117

Cite this article as: Frostegård, J. BMC Med 2013 11: 117. doi:10.1186-1741-7015-11-117


Atherosclerosis, the major cause of cardiovascular disease CVD, is a chronic inflammatory condition with immune competent cells in lesions producing mainly pro-inflammatory cytokines. Dead cells and oxidized forms of low density lipoproteins oxLDL are abundant. The major direct cause of CVD appears to be rupture of atherosclerotic plaques. oxLDL has proinflammatory and immune-stimulatory properties, causes cell death at higher concentrations and contains inflammatory phospholipids with phosphorylcholine PC as an interesting epitope. Antibodies against PC anti-PC may be atheroprotective, one mechanism being anti-inflammatory. Bacteria and virus have been discussed, but it has been difficult to find direct evidence, and antibiotic trials have not been successful. Heat shock proteins could be one major target for atherogenic immune reactions. More direct causes of plaque rupture include pro-inflammatory cytokines, chemokines, and lipid mediators. To prove that inflammation is a cause of atherosclerosis and CVD, clinical studies with anti-inflammatory and-or immune-modulatory treatment are needed. The potential causes of immune reactions and inflammation in atherosclerosis and how inflammation can be targeted therapeutically to provide novel treatments for CVD are reviewed.

KeywordsImmunity Atherosclerosis Cardiovascular disease Phosholipids Natural antibodies T-cells B-cells Inflammation AbbreviationsAAAggregatibacter actinomycetemcomitans

AGEsAdvanced glycation end products

anti-apo BAntibodies against apoprotein B

anti-PCAntibodies against phosphorylcholine

aOxCLAntibodies against oxidized forms of cardiolipin

aOxPSAntibodies against oxidized phosphatidylserine

beta2GPIBeta 2-glycoprotein I


CPChlamydia pneumoniae

CRPC-reactive protein

CVDCardiovascular disease

DAMPDanger associated molecular patterns

EBVEpstein-Barr virus

HPHelicobacter pylori

HSPHeat-shock proteins



IVIGIntravenous immunoglobulin

LDLLow density lipoprotein



MIMyocardial infarction

oxLDLOxidized low density lipoprotein

PAFPlatelet-activating factor

PAMPPathogen associated molecular patterns


PGPorphyromonas gingivalis

PLA2Phospholipase 2

RARheumatoid arthritis

SMCSmooth muscle cells

SLESystemic lupus erythematosus

TNFTumor necrosis factor.

Electronic supplementary materialThe online version of this article doi:10.1186-1741-7015-11-117 contains supplementary material, which is available to authorized users.

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Autor: Johan Frostegård


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