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Human Immunodeficiency Virus-1 Entry Into Purified Blood Dendritic Cells Through CC and CXC Chemokine Coreceptors
Seyoum Ayehunie,
Eduardo A. Garcia-Zepeda,
James A. Hoxie,
Richard Horuk,
Thomas S. Kupper,
Andrew D. Luster, and
Ruth M. Ruprecht
From the Laboratory of Viral Pathogenesis, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA; the Infectious Disease Unit, AIDS Research Center, Massachusetts General Hospital, Boston, MA; the Division of Hematology-Oncology, University of Pennsylvania, Philadelphia, PA; the Department of Immunology, Berlex Biosciences, Richmond, CA; and the Division of Dermatology, Brigham and Women's Hospital, Boston, MA.
Blood dendritic cells (DC) are susceptible to both macrophage (M) and T-cell line (T) tropic human immunodeficiency virus type 1. The CC chemokines RANTES, macrophage inflammatory protein-1 (MIP-1), MIP-1 , eotaxin, and, to a lesser extent, monocyte chemoattractant protein-1 (MCP-1) and MCP-4 blocked entry of M-tropic virus into blood DC. The CXC chemokine, SDF-1, a fusin (CXCR4 chemokine receptor) ligand, and an antifusin antibody inhibited DC entry by T-tropic virus. Purified blood DC contained CCR1, CCR2, CCR3, and CCR5 as well as the CXCR4 chemokine receptor RNA transcripts and high levels of fusin on the cell surface. The coexpression of multiple chemokine receptors offers a molecular mechanism to explain the permissiveness of DC for both M- and T-tropic viruses.
Blood, Vol. 90 No. 4 (August 15), 1997:
pp. 1379-1386
© 1997 by The American Society of Hematology.
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