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* Department of Pathology and Laboratory Medicine,
Wisconsin National Primate Research Center, University of Wisconsin-Madison, Madison, WI 53706; and
Department of Biological Sciences, University of South Carolina, Columbia, SC 29208
Killer Ig-like receptors (KIRs) are implicated in protection from multiple pathogens including HIV, human papillomavirus, and malaria. Nonhuman primates such as rhesus and cynomolgus macaques are important models for the study of human pathogens; however, KIR genetics in nonhuman primates are poorly defined. Understanding KIR allelic diversity and genomic organization are essential prerequisites to evaluate NK cell responses in macaques. In this study, we present a complete characterization of KIRs in Mauritian cynomolgus macaques, a geographically isolated population. In this study we demonstrate that only eight KIR haplotypes are present in the entire population and characterize the gene content of each. Using the simplified genetics of this population, we construct a model for macaque KIR genomic organization, defining four putative KIR3DL loci, one KIR3DH, two KIR2DL, and one KIR1D. We further demonstrate that loci defined in Mauritian cynomolgus macaques can be applied to rhesus macaques. The findings from this study fundamentally advance our understanding of KIR genetics in nonhuman primates and establish a foundation from which to study KIR signaling in disease pathogenesis.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by Grant R24 RR021745-01A1 from National Institutes of Health (NIH), Contract number HHSN266200400088C/N01-AI-40088 from the National Institute of Allergy and Infectious Diseases, and by the International AIDS Vaccine Initiative. B.N.B. received support from NIH National Research Service Award T32 GM007215 from the National Institute of General Medical Sciences. A.L.H. received support by Grant GM43940 from the NIH. This research was conducted in part at a facility constructed with support by Grants RR15459-01 and RR020141-01 from the Research Facilities Improvement Program.
2 Address correspondence and reprint requests to Dr. David H. O'Connor, Department of Pathology and Laboratory Medicine, 5440 Medical Sciences Center, University of Wisconsin-Madison, 1300 University Avenue, Madison, WI 53706. E-mail address: doconnor{at}primate.wisc.edu
3 Abbreviations used in this paper: KIR, killer Ig-like receptor; MCM, Mauritian cynomolgus macaques.
4 The online version of this article contains supplemental material.
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