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The notion that coronary atherosclerosis and its most severe phenotype, myocardial infarction (MI), are chronic inflammatory diseases is supported by several lines of evidence. Interleukins (ILs) are important mediators and modulators of inflammation. Specific polymorphisms in the genes encoding subunits of IL-23 ( IL-12B) and its receptor ( IL-23R) have recently been consistently found to be associated with chronic immune-mediated diseases. In this study, we explored the hypothesis that these variants also affect the risk of MI. We conducted a case–control association study on a cohort of 738 British Caucasian MI patients and 716 population controls. We tested four variants (rs11209026, rs7517847, rs1343151, rs10889677) of IL-23R and the A1188C polymorphism (rs3212227) of IL-12B. There was no association of any IL-23R (rs11209026, p = 0.82; rs7517847, p = 0.87; rs1343151, p = 0.85; rs10889677, p = 0.48) or IL-12B (rs3212227, p = 0.32) polymorphisms with MI. Stratification for age, gender and other cardiovascular risk factors did not affect the findings. These results indicate that unlike other chronic inflammatory diseases, the examined variants are unlikely to be major contributors to the pathogenesis of MI. [ABSTRACT FROM AUTHOR]