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炎症性肠病中杀伤细胞免疫球蛋白样受体基因及其 HLA 配体分析。

Analysis of Killer Cell Immunoglobulin-Like Receptor Genes and Their HLA Ligands in Inflammatory Bowel Diseases.

机构信息

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Rheumatology Expert Group (REG), Universal Scientific Education and Research Network (USERN), Tehran, Iran.

出版信息

J Immunol Res. 2020 Sep 19;2020:4873648. doi: 10.1155/2020/4873648. eCollection 2020.

Abstract

Genetic studies have illustrated that () genes could participate in various autoimmune disorders. We aimed to clarify the role of genes, ligands, HLA-KIR interactions, and their genotypes in inflammatory bowel disease (IBD) susceptibility. The study population was composed of 183 IBD subjects, comprising 100 ulcerative colitis (UC) patients, 83 Crohn's disease (CD) patients, and 274 healthy subjects. Polymerase chain reaction with sequence-specific primers (PCR-SSP) was used to evaluate the absence or presence of the 15 genes, 5 class I ligands, and 2 pseudogenes. We did not find any significant difference in allele frequency of and pseudogenes between IBD patients and healthy controls. In the case of genes, there was a significant difference in frequency between UC patients and healthy controls ( = 0.03, OR = 0.06, 95%CI = 0.008-0.4). Furthermore, we found a significant difference in frequency between CD patients and healthy controls ( = 0.04, OR = 0.49, 95% CI = 0.3-0.8). In the full-array combination of genes, there was no significant frequency difference between UC patients and healthy controls, while two KIR genotypes showed a significant susceptible association with CD. Our data do not support a strong role of NK cells in IBD susceptibility, but it does not rule out a role for KIR variability in IBD patients. However, there are some protective associations such as Bw4 alleles; these associations may be due to the interaction of the alleles to TCRs rather than KIRs.

摘要

遗传研究表明,()基因可能参与各种自身免疫性疾病。我们旨在阐明基因、配体、HLA-KIR 相互作用及其基因型在炎症性肠病 (IBD)易感性中的作用。研究人群由 183 例 IBD 患者组成,包括 100 例溃疡性结肠炎 (UC)患者、83 例克罗恩病 (CD)患者和 274 例健康对照。采用序列特异性引物聚合酶链反应 (PCR-SSP) 评估 15 个基因、5 个 I 类配体和 2 个假基因的缺失或存在情况。我们未发现 IBD 患者和健康对照组之间基因和假基因的等位基因频率有任何显著差异。在基因方面,UC 患者与健康对照组之间的频率存在显著差异(=0.03,OR=0.06,95%CI=0.008-0.4)。此外,我们发现 CD 患者与健康对照组之间的频率存在显著差异(=0.04,OR=0.49,95%CI=0.3-0.8)。在基因的全基因组合中,UC 患者与健康对照组之间无显著频率差异,而两种 KIR 基因型与 CD 具有显著的易感关联。我们的数据不支持 NK 细胞在 IBD 易感性中起重要作用,但不能排除 KIR 变异性在 IBD 患者中的作用。然而,存在一些保护相关性,例如 Bw4 等位基因;这些关联可能是由于等位基因与 TCR 而不是 KIR 的相互作用所致。

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