Several inflammatory markers have been implicated in coronary artery plaque destabilization and subsequent rupture. Interleukins, a group of cytokines, are recognized as crucial mediators involved in the host inflammatory response. Interleukin-10 (IL-10) which is secreted by Th2 cells and macrophages, is an important anti-inflammatory cytokine with potent deactivating properties on both macrophages and T cells. IL-10 is expressed in both early and advanced human atherosclerotic plaques and interplay between IL-12 and IL-10 seem to contribute to the level of immune-mediated tissue injury in atherosclerosis [1]. A significant 3-fold increase in lipid accumulation and a 30-fold increase in atherosclerotic lesion size was seen amongst IL-10 deficient mice as opposed to a wild-type mice, fed with an atherogenic diet and raised under different, specific conditions [2]. These atherosclerotic lesions amongst IL-10 deficient mice also showed marked increase in T-cell infiltration, interferon-ɣ (IFN-ɣ) expression, and decreased collagen content. High levels of IL-10 expression in atherosclerotic plaques has been associated with significant decrease in inducible nitric oxide synthase expression and cell death with further alludes to the anti-inflammatory properties of IL-10 [3]. IL-10 thus seems to be intricately involved in several processes involving plaque progression, rupture and subsequent thrombosis.

Human IL-10 gene resides in the long arm of chromosome 1 at position q31-32 [4], [5]. A single nucleotide polymorphism (SNP) at position −1082 bp in the IL-10 gene, involving a guanine (G) or adenine (A) substitution (rs1800896), has been reported to be associated with ≅ 32 % reduction in mean IL-10 production in vitro [6]. Significant association of this SNP was noted, at least via dominant genetic model comparisons, in two largest case-control studies on the subject, exclusively comprising of premature coronary artery disease (CAD) [7] and acute coronary syndrome patients [8], as compared to CAD-free controls. In contrast, certain sizable studies examining stable CAD patients showed either none [9] or negative associations [10]. We therefore sought to investigate a possible association of this SNP with acuity of presentations of CAD, brought about by IL-10 deficiency-mediated plaque destabilization. This aspect has not been investigated in earlier meta-analyses published on this subject [11], [12], [13], [14], [15], [16].

Against this background, we conducted an updated systematic review and meta-analysis of association studies in order to assess the association of IL-10-1082G/A with early or severe and non-severe presentation of CAD.