Review
The macrophage in HIV-1 infection: From activation to deactivation?
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* Corresponding author: Georges Herbein georges.herbein@univ-fcomte.fr
1 Department of Virology, UPRES EA 4266 Pathogens and Inflammation, IFR 133 INSERM, Franche-Comte University, CHU Besançon, Besançon, France
2 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA
Retrovirology 2010, 7:33 doi:10.1186/1742-4690-7-33
Published: 9 April 2010Abstract
Macrophages play a crucial role in innate and adaptative immunity in response to microorganisms and are an important cellular target during HIV-1 infection. Recently, the heterogeneity of the macrophage population has been highlighted. Classically activated or type 1 macrophages (M1) induced in particular by IFN-γ display a pro-inflammatory profile. The alternatively activated or type 2 macrophages (M2) induced by Th-2 cytokines, such as IL-4 and IL-13 express anti-inflammatory and tissue repair properties. Finally IL-10 has been described as the prototypic cytokine involved in the deactivation of macrophages (dM). Since the capacity of macrophages to support productive HIV-1 infection is known to be modulated by cytokines, this review shows how modulation of macrophage activation by cytokines impacts the capacity to support productive HIV-1 infection. Based on the activation status of macrophages we propose a model starting with M1 classically activated macrophages with accelerated formation of viral reservoirs in a context of Th1 and proinflammatory cytokines. Then IL-4/IL-13 alternatively activated M2 macrophages will enter into the game that will stop the expansion of the HIV-1 reservoir. Finally IL-10 deactivation of macrophages will lead to immune failure observed at the very late stages of the HIV-1 disease.