| http://purl.uniprot.org/citations/20802150 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20802150 | http://www.w3.org/2000/01/rdf-schema#comment | "Modulation of human NK cell function by killer cell Ig-like receptors (KIR) and MHC class I is dominated by the bipartite interactions of inhibitory lineage III KIR with the C1 and C2 epitopes of HLA-C. In comparison, the ligand specificities and functional contributions of the activating lineage III KIR remain poorly understood. Using a robust, sensitive assay of KIR binding and a representative panel of 95 HLA class I targets, we show that KIR2DS1 binds C2 with ~50% the avidity of KIR2DL1, whereas KIR2DS2, KIR2DS3, and KIR2DS5 have no detectable avidity for C1, C2, or any other HLA class I epitope. In contrast, the chimpanzee has activating C1- and C2-specific lineage III KIR with strong avidity, comparable to those of their paired inhibitory receptors. One variant of chimpanzee Pt-KIR3DS2, the activating C2-specific receptor, has the same avidity for C2 as does inhibitory Pt-KIR3DL4, and a second variant has ~73% the avidity. Chimpanzee Pt-KIR3DS6, the activating C1-specific receptor, has avidity for C1 that is ~70% that of inhibitory Pt-KIR2DL6. In both humans and chimpanzees we observe an evolutionary trend toward reducing the avidity of the activating C1- and C2-specific receptors through selective acquisition of attenuating substitutions. However, the extent of attenuation has been extreme in humans, as exemplified by KIR2DS2, an activating C1-specific receptor that has lost all detectable avidity for HLA class I. Supporting such elimination of activating C1-specific receptors as a uniquely human phenomenon is the presence of a high-avidity activating C1-specific receptor (Gg-KIR2DSa) in gorilla."xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1001951"xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/author | "Parham P."xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/author | "Abi-Rached L."xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/author | "Guethlein L.A."xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/author | "Graef T."xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/author | "Moesta A.K."xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/author | "Older Aguilar A.M."xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/pages | "4233-4237"xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/title | "Humans differ from other hominids in lacking an activating NK cell receptor that recognizes the C1 epitope of MHC class I."xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://purl.uniprot.org/core/volume | "185"xsd:string |
| http://purl.uniprot.org/citations/20802150 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20802150 |
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