Journal
HUMAN IMMUNOLOGY
Volume 71, Issue 1, Pages 1-13Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2009.08.011
Keywords
HIV-1; Macrophages; T(h)2; Cytokines; Transmission
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Funding
- Agence Nationale de Recherches sur le SIDA et les hepatites virales (ANRS)
- Institut National de la Sante et de la Recherche Medicale (INSERM), France
- VIdegrees PCRD
- ANRS
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Macrophages constitute major human immunodeficiency virus type 1 (HIV-1) reservoirs at the mucosal level and their functional activity is modulated by cytokine environments that could play a role in HIV-1 mucosal spread. As proof of concept, we herein evaluated the modulation of HIV/macrophages interactions associated With two ubiquitous T(h)2 cytokines, namely, interleukin (IL)-4 and IL-13, using the in vitro model of R5-HIV-1 transfer from macrophages to T lymphocytes. Monocyte-derived macrophages differentiated in the presence of IL-4 (M-4) transferred the virus to T cells more efficiently than those differentiated in the presence of interleukin-13 (M-13), likely because to their high capacity to capture and produce HIV-1 and to recruit HIV-1 target T cell. However, M-13 harbored high levels of HIV DNA, similarly to M-4, and secreted HIV-activating factors. Notably, uninfected macrophages recruited HIV-1 target T cells (CCR4(+)IL-13(+) T(h)2 cells and CD4(+)CCR5(+) T cells), indicating their role in facilitating the HIV-1 spread by a passive manner. Strikingly, R5-HIV-1 reprogrammed macrophages toward a T(h)1 secretion pattern. Thus, T(h)2 microenvironment facilitates the emergence of HIV-1 macrophage reservoir and HIV-1 spread. In conclusion, secreted cytokines within mucosae may differentially influence both the HIV-1 production within the mucosal target cells reservoir and its spread thorough the mucosal tissue. (C) 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
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