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Detection of KIR3DS1 on the Cell Surface of Peripheral Blood NK Cells Facilitates Identification of a Novel Null Allele and Assessment of KIR3DS1 Expression during HIV-1 Infection^1,2

Véronique Pascal^*, Eriko Yamada^*, Maureen P. Martin, Galit Alter, Marcus Altfeld, Julia A. Metcalf, Michael W. Baseler^¶, Joseph W. Adelsberger^¶, Mary Carrington, Stephen K. Anderson^*, and Daniel W. McVicar^3,*

^* Cancer and Inflammation Program, Laboratory of Experimental Immunology, Center for Cancer Research, National Cancer Institute-Frederick, Frederick, MD 21702; Basic Research Program, SAIC-Frederick Inc, National Cancer Institute-Frederick, Frederick, MD 21702; Partners AIDS Research Center, Infectious Disease Unit, Massachusetts General Hospital and Division of AIDS, Harvard Medical School, Boston, MA 02115; Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and ^¶ AIDS Monitoring Laboratory, Clinical Services Program, SAIC-Frederick, National Cancer Institute-Frederick, Frederick, MD 21702

KIR3DL1 is a highly polymorphic killer cell Ig-like receptor gene with at least 23 alleles described, including its activating counterpart, KIR3DS1. Recently, the KIR3DS1 allele has been shown to slow progression to AIDS in individuals expressing HLA-Bw4 with isoleucine at position 80. However, due to the lack of a specific Ab, KIR3DS1 expression and function is not well characterized. In this study, we demonstrate KIR3DS1 expression on a substantial subset of peripheral natural killer cells through its recognition by the mAb Z27. The fidelity of this detection method was confirmed by analysis of KIR3DS1 transfectants and the identification of a novel KIR3DS1 null allele. Interestingly, KIR3DS1 is also expressed by a small proportion of CD56⁺ T cells. We show that ligation of KIR3DS1 by Z27 leads to NK cell IFN- production and degranulation as assessed by expression of CD107a. Furthermore, we document the persistence of KIR3DS1⁺ NK cells in HIV-1 viremic patients. The high frequency of KIR3DS1 expression, along with its ability to activate NK cells, and its maintenance during HIV-1 viremia are consistent with the epidemiological data suggesting a critical role for this receptor in controlling HIV-1 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 project has been funded in whole or in part with federal funds from the National Cancer Institute, the Intramural Research Program of the National Institute of Allergy and Infectious Diseases and the National Institutes of Health, under Contract DHHS N01-C0-12400 and 1 R01 AI067031-01A2. This research was supported in part by the Intramural Research Program of the National Institutes of Health, National Cancer Institute, Center for Cancer Research.

² The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government. By acceptance of this article, the publisher or recipient acknowledges the right of the U.S. government to retain a nonexclusive, royalty-free license in and to any copyright covering the article.

³ Address correspondence and reprint requests to Dr. Daniel W. McVicar, National Cancer Institute-Frederick, Building 560/Room 31-46, Frederick, MD 21702. E-mail address: mcvicar{at}nih.gov

⁴ Abbreviations used in this paper: KIR, killer Ig-like receptor; MFI, mean channel fluorescence intensity.

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