Galectin-2 3279TT variant protects against the lymphotoxin-α 252GG genotype associated ischaemic stroke

ObjectiveThe galectin-2 protein is presumed to play a regulatory role in the intracellular trafficking of the lymphotoxin-α (LTA) cytokine. LTA is a pro-inflammatory factor, its 252GG homozygote variant is considered as a susceptibility factor for arteriosclerosis and cardiovascular diseases. By contrast, the galectin-2-encoding gene LGALS2 3279TT homozygote variant has been demonstrated to exert protection against myocardial infarction by reducing the transcriptional level of galectin-2, thereby leading to a reduced extracellular secretion of LTA.MethodsIn the present study, we examined whether the LGALS2 3279TT homozygote variant alone can influence the prevalence of ischaemic stroke, and whether it can interact somehow with the disadvantageous LTA 252GG homozygote variant. Genetic and clinical data of 385 ischemic stroke patients and 303 stroke and neuroimaging alteration-free controls were analysed.ResultsThe combination of the LGALS2 3279TT and LTA 252GG homozygote was significantly less frequent in the ischemic stroke group (1.56%) than in the controls (5.94%, p < 0.00187; overall stroke group: crude OR: 0.25, 95% CI: 0.1–0.64; adjusted OR: 0.03, 95% CI: 0.025–0.71).ConclusionsThis finding suggests a gene–gene interaction.