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CD4 Expression on Activated NK Cells: Ligation of CD4 Induces Cytokine Expression and Cell Migration¹

Helene B. Bernstein^2,*, Mary C. Plasterer^*, Sherrie E. Schiff^*, Christina M. R. Kitchen, Scott Kitchen and Jerome A. Zack^,

^* Department of Obstetrics and Gynecology, Department of Medicine, and Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, and Department of Biostatistics, School of Public Health, University of California, Los Angeles, CA 90095

NK cells play an important role in the innate immune response. We have isolated NK cells from human lymphoid tissues and found that these cells express the CD4 molecule on their surface at levels higher than those found on peripheral blood NK cells. To study the functional role of the CD4 molecule on NK cells, we developed an in vitro system by which we are able to obtain robust CD4 expression on NK cells derived from blood. CD4⁺ NK cells efficiently mediate NK cell cytotoxicity, and CD4 expression does not appear to alter lytic function. CD4⁺ NK cells are more likely to produce the cytokines -IFN and TNF- than are CD4^– NK cells. Ligation of CD4 further increases the number of NK cells producing these cytokines. NK cells expressing CD4 are also capable of migrating toward the CD4-specific chemotactic factor IL-16, providing another function for the CD4 molecule on NK cells. Thus, the CD4 molecule is present and functional on NK cells and plays a role in innate immune responses as a chemotactic receptor and by increasing cytokine production, in addition to its well-described function on T cells as a coreceptor for Ag responsive cell activation.

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 is supported by a grant from the National Institute of Allergy and Infectious Diseases, National Institutes of Health (1 R21 AI58786). H.B.B. is a Building Interdisciplinary Research Careers in Women’s Health Center Scholar (5 K12 HD01400).

² Address correspondence and reprint requests to Dr. Helene B. Bernstein, Department of Obstetrics and Gynecology, David Geffen School of Medicine at University of California, Los Angeles, 10833 Le Conte Avenue, CHS 22-150, Los Angeles, CA 90095-1740. E-mail address: hbernstein{at}mednet.ucla.edu

³ Abbreviations used in this paper: KIR, killer Ig-like receptor; MHC I, MHC class I; MHC II, MHC class II; 7AAD, 7-aminoactinomycin D; TREC, TCR-rearrangement excision circle; SDF-1, stromal-derived factor 1.