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Interferon- Increases Expression of Chemokine Receptors CCR1,
CCR3, and CCR5, But Not CXCR4 in Monocytoid U937 Cells
Davide Zella,
Oxana Barabitskaja,
Jennifer M. Burns,
Fabio Romerio,
Daniel E. Dunn,
Maria Grazia Revello,
Giuseppe Gerna,
Marvin S. Reitz Jr,
Robert C. Gallo, and
Frank F. Weichold
From the Institute of Human Virology and the Department of
Microbiology and Immunology, University of Maryland, Baltimore, MD; the
Hematology
Branch, National Heart, Lung and Blood Institute, National Institutes of
Health, Bethesda, MD; and the Viral Diagnostic Service, IRCCS
Policlinico S. Matteo, Pavia, Italy.
Chemokine receptors (CR), which can mediate migration of immune
cells to the site of inflammation, also function as coreceptors for
human immunodeficiency virus (HIV) entry into CD4+ T
lymphocytes and antigen-presenting cells. We demonstrate here that
interferon- (IFN-) increases the expression of chemokine receptors CCR1, CCR3, and CCR5 in monocytoid U937 cells as detected by
cell surface molecule labeling and mRNA expression, as well as by
intracellular calcium mobilization and cell migration in response to
specific ligands. The increased expression of these chemokine receptors
also results in an enhanced HIV-1 entry into cells. Our data provide
evidence for a relationship of cellular pathways that are induced by
IFN- with those that regulate chemokine receptor expression.
Blood, Vol. 91 No. 12 (June 15), 1998:
pp. 4444-4450
© 1998 by The American Society of Hematology.
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