Genetic studies have illustrated that killer cell immunoglobulin-like receptor (KIR) genes could participate in various autoimmune disorders. We aimed to clarify the role of KIR genes, HLA 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 KIR genes, 5 HLA class I ligands, and 2 pseudogenes. We did not find any significant difference in allele frequency of KIRs and pseudogenes between IBD patients and healthy controls. In the case of HLA genes, there was a significant difference in HLA-B-Bw4^Thr80 frequency between UC patients and healthy controls (, , -0.4). Furthermore, we found a significant difference in HLA-C1^Asn80 frequency between CD patients and healthy controls (, , 95% -0.8). In the full-array combination of KIR 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.

中文翻译：

---

炎性肠病中杀伤细胞免疫球蛋白样受体基因及其HLA配体的分析

遗传研究表明，杀伤细胞免疫球蛋白样受体（KIR）基因可能参与多种自身免疫性疾病。我们旨在阐明在炎症性肠病（IBD）易感性中KIR基因，HLA配体，HLA-KIR相互作用及其基因型的作用。研究人群由183名IBD受试者组成，包括100名溃疡性结肠炎（UC）患者，83克罗恩氏病（CD）患者和274名健康受试者。聚合酶链反应与序列特异性引物（PCR-SSP）用于评估15个KIR基因，5个HLA是否存在I类配体和2个假基因。我们没有发现IBD患者和健康对照之间的KIR和假基因等位基因频率有任何显着差异。就HLA基因而言，UC患者与健康对照组之间的HLA-B-Bw4 ^Thr80频率存在显着差异（， ， - 0.4）。此外，我们发现CD患者与健康对照组之间的HLA-C1 ^Asn80频率存在显着差异（， ， 95％- 0.8）。在KIR基因的全阵列组合中，UC患者和健康对照之间没有明显的频率差异，而两种KIR基因型显示出与CD的显着易感性关联。我们的数据不支持NK细胞在IBD易感性中的重要作用，但不排除IBD患者KIR变异性的作用。但是，有一些保护性关联，例如Bw4等位基因；这些关联可能是由于等位基因与TCR而非KIR的相互作用。