title: Assessment of killer cell immunoglobulinlike receptor expression and corresponding HLA class I phenotypes demonstrates heterogenous KIR expression independent of anticipated HLA class I ligands.
abstract: Natural killer (NK) cell-mediated cytolysis is stimulated and downregulated through the interaction of distinct human leukocyte antigen (HLA) class I molecules on target cells with specific killer cell immunoglobulinlike receptors (KIRs) on NK cells. Killer cell immunoglobulinlike receptors are highly polymorphic and are clonally distributed on NK cell populations within individuals. However, the regulation of KIR expression by individual HLA class I phenotypes is not well understood. To examine a potential influence of the HLA class I phenotype on KIR expression patterns we studied the KIR expression in individuals that were subgrouped according to the major HLA-C encoded KIR-epitopes (group C1 versus C2). In these individuals, NK cells were analyzed for KIR expression using flow cytometry and RNA-based expression analysis. Our results demonstrate that KIR genes are transmitted very heterogeneously with two main patterns of KIR genotypes as previously described; group A and group B (with 21 different genotypes). There are distinct populations exhibiting different densities of CD158a and/or CD158b positive NK cells that coexist in all individuals. A clear correlation between KIR expression and the currently known HLA class I ligands was not observed. In conclusion, the surface expression of KIRs in individuals with different HLA class I genotypes indicates that other non-HLA class I encoded factors contribute to the shaping of the KIR repertoire.
authors.affiliation: Institute of Transfusion Medicine and Immunohematology, RCBDS, Frankfurt, Germany.
authors.forename: Sven
authors.initials: S
authors.lastname: Becker
authors.forename: Torsten
authors.initials: T
authors.lastname: Tonn
authors.forename: Tobias
authors.initials: T
authors.lastname: Füssel
authors.forename: Markus
authors.initials: M
authors.lastname: Uhrberg
authors.forename: Manuela
authors.initials: M
authors.lastname: Bogdanow
authors.forename: Erhard
authors.initials: E
authors.lastname: Seifried
authors.forename: Christian
authors.initials: C
authors.lastname: Seidl
mesh_terms: D001782:Blood Donors; D020090:Chromosome Segregation; D002888:Chromosomes, Human, Pair 19 / Q000235:genetics; D002896:Chromosomes, Human, Pair 6 / Q000235:genetics; D002999:Clone Cells / Q000378:metabolism; D005786:Gene Expression Regulation; D005787:Gene Frequency; D005838:Genotype; D005858:Germany; D006239:Haplotypes / Q000235:genetics; D015395:Histocompatibility Antigens Class I / Q000235:genetics*; D006650:Histocompatibility Testing; D006801:Humans; D007694:Killer Cells, Natural / Q000145:classification / Q000378:metabolism; D008024:Ligands; D015810:Linkage Disequilibrium; D010641:Phenotype; D011971:Receptors, Immunologic / Q000096:biosynthesis / Q000235:genetics*; D054340:Receptors, KIR; D054342:Receptors, KIR2DL1; D054344:Receptors, KIR2DL3; D044465:White People / Q000235:genetics
chemical_list: D015395:Histocompatibility Antigens Class I; D008024:Ligands; D011971:Receptors, Immunologic; D054340:Receptors, KIR; D054342:Receptors, KIR2DL1; D054344:Receptors, KIR2DL3