Distribution of KIR genes in the population of unrelated individuals homozygous for ancestral haplotype AH8.1 (HLA-A1B8DR3)
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
20492596
DOI
10.1111/j.1399-0039.2010.01504.x
PII: TAN1504
Knihovny.cz E-resources
- MeSH
- DNA analysis genetics MeSH
- Gene Frequency MeSH
- Genotype MeSH
- Haplotypes genetics MeSH
- HLA Antigens genetics MeSH
- Homozygote MeSH
- Humans MeSH
- Polymerase Chain Reaction MeSH
- Population Groups genetics MeSH
- Receptors, KIR genetics MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- DNA MeSH
- HLA Antigens MeSH
- Receptors, KIR MeSH
Despite the independent segregation of genes encoding killer immunoglobulin-like receptor (KIR) and human leukocyte antigen (HLA), there is some evidence of some kind of co-evolution. Therefore, one could expect reduced KIR diversity within the HLA restricted population. A total of 41 unrelated individuals homozygous for ancestral HLA haplotype AH8.1 (HLA-A*0101-Cw*0701-B*0801-DRB1*0301-DQB1*0201) were genotyped for KIRs. Over all, 14 different genotypes were identified. The KIR genes and genotypes repertoire generally mirror the published frequencies in Caucasians. Except for KIR2DS4, all activating genes presented frequencies below 50%. KIR2DS5 was the least frequent among activating genes (17%), whereas KIR2DL5 (37%) among inhibitory ones. The most frequent (39%) was AA genotype. Twenty-two individuals (54%) had a copy of KIR haplotypes A and B (AB genotype), whereas three (7%) were homozygous for B (BB genotype). Nine of fourteen reported genotypes occurred only in one individual. Five genotypes were reported in less than twenty individuals worldwide and one genotype was reported so far only once. Conversely, the three most frequent genotypes account for 68% of all detected genotypes. The results show the unrestricted KIR diversity in this HLA uniform group and support the fact that the driving force for KIR evolution is not exclusively a major histocompatibility complex.
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