The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/2/439/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 3, February 2, 1998 439-444

Brief Definitive Reports

Interleukin 10 Increases CCR5 Expression and HIV Infection in Human Monocytes

Silvano Sozzani*, Silvia Ghezzi{ddagger}, Gioacchino Iannolo*, Walter Luini*, Alessandro Borsatti*, Nadia Polentarutti*, Antonio Sica*, Massimo Locati*, Charles Mackay, Timothy N.C. Wells§, Priscilla Biswas{ddagger}, Elisa Vicenzi{ddagger}, Guido Poli{ddagger}, and Alberto Mantovani*,||

From the * Istituto di Ricerche Farmacologiche ‘Mario Negri', 20157 Milan, Italy; {ddagger} the AIDS Immunopathogenesis Unit, San Raffaele Scientific Institute, 20132 Milan, Italy; § the Geneva Biomedical Research Institute, Glaxo Wellcome Research and Development, Geneva, Switzerland; || the Section of Pathology and Immunology, Department of Biotechnology, University of Brescia, 25123 Brescia, Italy; and Millennium Biotherapeutics Inc., Cambridge, MA

The immunosuppressive and antiinflammatory cytokine interleukin (IL) 10 selectively upregulates the expression of the CC chemokine receptors CCR5, 2, and 1 in human monocytes by prolonging their mRNA half-life. IL-10–stimulated monocytes display an increased number of cell surface receptors for, and better chemotactic responsiveness to, relevant agonists than do control cells. In addition, IL-10–stimulated monocytes are more efficiently infected by HIV BaL. This effect was associated to the enhancement of viral entry through CCR5. These data add support to an emerging paradigm in which pro- and antiinflammatory molecules exert reciprocal and opposing influence on chemokine agonist production and receptor expression.

Address correspondence to Dr. Alberto Mantovani, Istituto di Ricerche Farmacologiche ‘Mario Negri', via Eritrea 62, 20157 Milan, Italy. Phone: 39-2-3901-4493; Fax: 39-2-354-6277; E-mail: mantovani{at}irfmn.mnegri.it

S. Sozzani and S. Ghezzi contributed equally to this work.


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