The Journal of Experimental Medicine
Janeway's Immunobiology 7th Edition
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Published 4 August 2003. doi:10.1084/jem.20022018
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© Rockefeller University Press, 0022-1007/2003/8/443 $5.00
The Journal of Experimental Medicine, Volume 198, Number 3, 443-453

CSF-induced and HIV-1–mediated Distinct Regulation of Hck and C/EBPß Represent a Heterogeneous Susceptibility of Monocyte-derived Macrophages to M-tropic HIV-1 Infection

Iwao Komuro1,2, Yasuko Yokota1, Sachiko Yasuda1, Aikichi Iwamoto2 and Kiyoko S. Kagawa1

1 Department of Immunology, National Institute of Infectious Disaeses, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan
2 Division of Infectious Diseases, Advanced Clinical Research Center, Institute of Medical Science, University of Tokyo, Shiroganedai 4-6-1, Minato-ku, Tokyo 108-8639, Japan

Address correspondence to K.S. Kagawa, Department of Immunology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan. Phone: 81-3-5285-1111; Fax: 81-3-5285-1150; email: akagawak{at}nih.go.jp

Granulocyte/macrophage colony-stimulating factor (GM-CSF)–induced monocyte-derived macrophages (GM-M{Phi}) are permissive to M-tropic HIV-1 entry, but inhibit viral replication at posttranscriptional and translational levels, whereas M-CSF-induced macrophages (M-M{Phi}) produce a large amount of HIV-1. M-M{Phi} express a high level of Hck and a large isoform of C/EBPß, and HIV-1 infection increases the expression of Hck but not of C/EBPß. GM-M{Phi} express a high level of C/EBPß and a low level of Hck, and HIV-1 infection drastically increases the expression of a short isoform of C/EBPß but decreases that of Hck.

Treatment of M-M{Phi} with antisense oligonucleotide for Hck (AS-Hck) not only suppresses the expression of Hck, but also stimulates the induction of the short isoform of C/EBPß and inhibits the viral replication. Treatment of GM-M{Phi} with a moderate amount of AS-C/EBPß not only inhibits the expression of the small isoform of C/EBPß preferentially, but also stimulates the induction of Hck and stimulates the virus production at a high rate. These results suggest that CSF-induced and HIV-1–mediated distinct regulation of Hck and small isoform of C/EBPß represent the heterogeneous susceptibility of tissue M{Phi} to HIV-1 infection, and the regulation of Hck and C/EBPß are closely related and these two molecules affect one another.

Key Words: macrophages • HIV-1 • Hck • C/EBPß • CSF


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