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A more recent version of this article appeared on February 1, 2006

Published online before print November 21, 2005
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0705382

Received for publication July 11, 2005.
Revised September 5, 2005.
Accepted for publication October 7, 2005.

Article

Phagocytosis stimulates mobilization and shedding of intracellular CD16A in human monocytes and macrophages: inhibition by HIV-1 infection

Nicole L. Webster *{dagger}@, Katherine Kedzierska *{ddagger}, Rula Azzam *{sect}, Geza Paukovics *, John Wilson , Suzanne M. Crowe *{sect}, and Anthony Jaworowski *{sect}

*AIDS Pathogenesis Research Program, Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, Australia; Departments of {dagger}Immunology and {sect}Medicine, Monash University, Melbourne, Australia; {ddagger}Department of Microbiology and Immunology, University of Melbourne, Australia; and Respiratory Unit, The Alfred Hospital, Melbourne, Australia

@ To whom correspondence should be addressed. E-mail: nwebster{at}burnet.edu.au.


  Abstract

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{gamma}R • immunoglobulin G




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N. L. Webster and S. M. Crowe
Matrix metalloproteinases, their production by monocytes and macrophages and their potential role in HIV-related diseases
J. Leukoc. Biol., November 1, 2006; 80(5): 1052 - 1066.
[Abstract] [Full Text] [PDF]


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