Phagocytosis stimulates mobilization and shedding of intracellular CD16A in human monocytes and macrophages: inhibition by HIV-1 infection.
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.
Webster
Nicole L
NL
Macfarlane Burnet Institute for Medical Research and Public Health, 85 Commercial Rd., Melbourne 3004, Australia. nwebster@burnet.edu.au
Kedzierska
Katherine
K
Azzam
Rula
R
Paukovics
Geza
G
Wilson
John
J
Crowe
Suzanne M
SM
Jaworowski
Anthony
A
D002478:Cells, Cultured; D005434:Flow Cytometry / Q000379:methods; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D066298:In Vitro Techniques; D008264:Macrophages / Q000276:immunology* / Q000821:virology; D009000:Monocytes / Q000276:immunology* / Q000821:virology; D010587:Phagocytosis / Q000276:immunology*; D017452:Receptors, IgG / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology
C496124:FCGR3A protein, human; D017452:Receptors, IgG