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Analysis of Killer Cell Immunoglobulin-Like Receptor Genes and Their Hla Ligands in Inflammatory Bowel Diseases Publisher Pubmed



Beigmohammadi F1 ; Mahmoudi M1, 2, 3 ; Karami J1, 4 ; Ahmadzadeh N1 ; Ebrahimidaryani N5 ; Rezaei N6, 7, 8
Authors
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Authors Affiliations
  1. 1. Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Rheumatology Expert Group (REG), Universal Scientific Education and Research Network (USERN), Tehran, Iran
  3. 3. Inflammation Research Center, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Gastroenterology and Hepatology, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran

Source: Journal of Immunology Research Published:2020


Abstract

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-Bw4Thr80 frequency between UC patients and healthy controls (P=0.03, OR=0.06, 95%CI=0.008-0.4). Furthermore, we found a significant difference in HLA-C1Asn80 frequency between CD patients and healthy controls (P=0.04, OR=0.49, 95% CI=0.3-0.8). 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. © 2020 Fereshteh Beigmohammadi et al.
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