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Published online before print November 21, 2005
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,1



* AIDS Pathogenesis Research Program, Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, Australia; Departments of
Immunology and
Medicine, Monash University, Melbourne, Australia;
Department of Microbiology and Immunology, University of Melbourne, Australia; and
¶ Respiratory Unit, The Alfred Hospital, Melbourne, Australia
1Correspondence: AIDS Pathogenesis and Clinical Research Program, Macfarlane Burnet Institute for Medical Research and Public Health, 85 Commercial Rd., Melbourne 3004, Australia. E-mail: nwebster{at}burnet.edu.au
Surface and intracellular staining coupled with flow cytometric analysis was used to show for the first time that human macrophages and a minor subset of peripheral blood monocytes have an internal pool of CD16A, which is mobilized and shed during Fc receptor for immunoglobulin G-mediated phagocytosis. Human immunodeficiency virus type 1 (HIV-1) infection of monocyte-derived macrophages in vitro led to a reduction in the phagocytosis-induced up-regulation in CD16A shedding. These results suggest that monocytes and macrophages may be a source of soluble CD16A, which is elevated in the serum of patients in a variety of disease states and that the mobilization and shedding of CD16A in response to phagocytosis are disrupted by HIV-1 infection.
Key Words: soluble CD16 Fc
R immunoglobulin G soluble Fc
RIII monocyte subsets
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