Killer-cell immunoglobulin-like receptor and human leukocyte antigen-C genes in common variable immunodeficiency
Autor: | Abdullah Baysan, Mustafa Gulec, Rahsan Ilikci Sagkan, Özgür Kartal, Sait Yesillik, Ali Selcuk, Ugur Musabak, Aysel Pekel, Osman Şener, Fevzi Demirel |
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Rok vydání: | 2015 |
Předmět: |
Adult
Genetic Markers Male 0301 basic medicine Turkey KIR Ligand Killer-cell immunoglobulin-like receptor HLA-C Antigens Human leukocyte antigen Polymorphism Single Nucleotide Pathogenesis Young Adult 03 medical and health sciences 0302 clinical medicine Receptors KIR Risk Factors Prevalence medicine Humans Genetic Predisposition to Disease Allele Receptor Allele frequency Genetic Association Studies business.industry Common variable immunodeficiency General Medicine medicine.disease Common Variable Immunodeficiency 030104 developmental biology Immunology Female business 030215 immunology |
Zdroj: | Wiener klinische Wochenschrift. 128:822-826 |
ISSN: | 1613-7671 0043-5325 |
Popis: | We aimed herein to investigate the killer-cell immunoglobulin-like receptor (KIR) genes and human leukocyte antigen (HLA)-C alleles in patients with common variable immunodeficiency (CVID), and to reveal their differences from those in healthy population. In all, 18 patients who have been diagnosed with CVID and 15 living donors of kidney transplant recipients were enrolled in the study. Polymerase chain reaction-sequence-specific primer (PCR-SSP) typing method was used in molecular genetic analysis. The frequencies of the genes in the study groups were statistically compared with each other using chi-square or Fisher exact tests, whichever were appropriate. Although there was no significant difference between both study groups with respect to distribution of KIR and HLA-C2 group genes, HLA-Cw7 allele frequency in patients with CVID was significantly lower than that in healthy population (P = 0.008). This present study results support that HLA-Cw7 allele, an inhibitor of KIR ligand, may play a role in the pathogenesis of CVID. |
Databáze: | OpenAIRE |
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