caa a22 4500 467907447 CHVBK 20180406152838.0 cr unu---uuuuu 170328e20060601xx s 000 0 eng 10.1007/s00251-006-0108-3 doi (NATIONALLICENCE)springer-10.1007/s00251-006-0108-3 High KIR diversity in Amerindians is maintained using few gene-content haplotypes [Elektronische Daten] [Ketevan Gendzekhadze, Paul Norman, Laurent Abi-Rached, Zulay Layrisse, Peter Parham] Interaction between killer cell immunoglobulin-like receptors (KIR) and cognate HLA class I ligands influences the innate and adaptive immune response to infection. The KIR family varies in gene content and allelic polymorphism, thereby, distinguishing individuals and populations. KIR gene content was determined for 230 individuals from three Amerindian tribes from Venezuela: the Yucpa, Bari and Warao. Gene-content haplotypes could be assigned to 212 individuals (92%) because only five different haplotypes were present—group A and four group B. Six different haplotype combinations accounted for >80% of individuals. Each tribe has distinctive genotype frequencies. Despite few haplotypes, all 14 KIR genes are at high frequency in the three tribes, with the exception of 2DS3. Each population has an even frequency of group A and B haplotypes. Allele-level analysis of 3DL1/S1 distinguished five group A haplotypes and six group B haplotypes. The high frequency and divergence of the KIR haplotypes in the Amerindian tribes provide greater KIR diversity than is present in many larger populations. An extreme case being the Yucpa, for whom two gene-content haplotypes account for >90% of the population. These comprise the group A haplotype and a group B haplotype containing all the KIR genes, except 2DS3, that typify the group B haplotypes. Here is clear evidence for balancing selection on the KIR system and the biological importance of both A and B haplotypes for the survival of human populations. Springer-Verlag, 2006 KIR haplotypes nationallicence KIR locus genotypes nationallicence Amerindians nationallicence Balancing selection nationallicence Gendzekhadze Ketevan Department of Structural Biology, Stanford University School of Medicine, Sherman Fairchild Building, Stanford, CA, USA aut Norman Paul Department of Structural Biology, Stanford University School of Medicine, Sherman Fairchild Building, Stanford, CA, USA aut Abi-Rached Laurent Department of Structural Biology, Stanford University School of Medicine, Sherman Fairchild Building, Stanford, CA, USA aut Layrisse Zulay Lab. Physiopathology, Experimental Medicine "Miguel Layrisse” Venezuelan Research Institute (IVIC), Caracas, Venezuela aut Parham Peter Department of Structural Biology, Stanford University School of Medicine, Sherman Fairchild Building, Stanford, CA, USA aut Immunogenetics Springer-Verlag 58/5-6(2006-06-01), 474-480 0093-7711 58:5-6<474 2006 58 251 https://doi.org/10.1007/s00251-006-0108-3 text/html Onlinezugriff via DOI 1 brief-communication jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00251-006-0108-3 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Gendzekhadze Ketevan Department of Structural Biology, Stanford University School of Medicine, Sherman Fairchild Building, Stanford, CA, USA aut NATIONALLICENCE 700 1- Norman Paul Department of Structural Biology, Stanford University School of Medicine, Sherman Fairchild Building, Stanford, CA, USA aut NATIONALLICENCE 700 1- Abi-Rached Laurent Department of Structural Biology, Stanford University School of Medicine, Sherman Fairchild Building, Stanford, CA, USA aut NATIONALLICENCE 700 1- Layrisse Zulay Lab. Physiopathology, Experimental Medicine "Miguel Layrisse” Venezuelan Research Institute (IVIC), Caracas, Venezuela aut NATIONALLICENCE 700 1- Parham Peter Department of Structural Biology, Stanford University School of Medicine, Sherman Fairchild Building, Stanford, CA, USA aut NATIONALLICENCE 773 0- Immunogenetics Springer-Verlag 58/5-6(2006-06-01), 474-480 0093-7711 58:5-6<474 2006 58 251 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer