Background: T-cells expressing the KIR2DS2 activating receptor werefound to be prevalent in the coronary culprit atherosclerotic plaque inpatients with acute coronary syndromes (ACS), suggesting a possiblecytolytic activity against the endothelium of the plaque, leading to plaquerupture and in turn to superimposed thrombosis and sudden occlusion ofthe artery. To explore if a similar pathogenetic mechanism occurs in acuteischemic stroke, we analyzed the possible association between thegenetic KIR and HLA repertoire and the susceptibility to ischemic stroke.Methods: Fourteen patients with ischemic stroke and ten controls withatherosclerotic disease without ischemic stroke matched for sex and agewere genotyped for KIR and their HLA ligands, using PCR-SSP.Results: The frequency of the homozygous A haplotype (only KIR2DS4as activating KIR) was 57% in patients and 80% controls (OR=0.33). Thetotal number of activating and inhibitory KIR was not significantly differentbetween cases and controls. The HLA-A was present in four cases andone control. The HLABw4T and HLABw4I alleles, as well as either thehomozygous or the heterozygous form, were present in 12 cases and 6controls, respectively. The putative interaction between HLABw4T/I alleleand the KIR3DL1 inhibitory receptor was reported in 12 cases and 6controls (OR=4).Conclusions: This descriptive preliminary analysis shows that subjectswith ischemic stroke have a lower frequency of the A-haplotype, a higherfrequency the HLABw4T or HLABw4I allele and a higher frequency of theHLABw4T/I-KIR3DL1 inhibitory interaction compared to controls,suggesting a stronger potential inhibition on NK activation.
|Numero di pagine||1|
|Rivista||THE AMERICAN JOURNAL OF PATHOLOGY|
|Stato di pubblicazione||Published - 2014|