Relationship between cerebrovascular diseases and human leukocyte antigen subgroups

Abstract

Abstract Purpose: Ischemic stroke is classified as large artery atherosclerosis, small vessel occlusion (lacunar infarcts), ischemic stroke due to other identified causes, and cryptogenic. The human leukocyte antigen (HLA) complex is a group of genes on chromosome six in humans responsible for encoding cell-surface proteins that regulate the immune system. In this study, HLA’s roles in the pathophysiology of ischemic stroke, especially the lacunar subgroup, are investigated, and their potential mechanisms are presented. Materials and methods: This study consisted of 49 patients with ischemic stroke and 50 healthy participants. HLA-A, HLA-B, HLA-C, HLA-DQB, and HLA-DRB subgroup genomes were assessed. Results: A statistically significant difference in the presence of HLA-A, HLA-B, HLA-C, HLA-DQB, and HLADRB subgroups was found between the control and patient groups. The presence of HLA-A*02, HLA-A*30, HLA-B*08, HLA-B*15, and HLA-DQB*06 genomes was higher in the patient group than in the control group (p≤0.05). Nevertheless, HLA-DQB*03 and HLA-DRB*11 genomes were found more in the control group than the patient group (p≤0.05) Conclusion: The results of this study pioneered in scrutinizing HLA alleles in small vascular disease (SVD). HLA-A*01, HLA-A*30, HLA-B*08, HLA-B*15, HLA-DQB*06, HLA-DQB*03 and HLA-DRB*11 are associated with HLA alleles of stroke patients with small vessel occlusion. We attempted to provide objective evidence for whether HLA genomes could act as a discriminative factor between SVD patients and control groups, which might hold considerable promise for future therapies.