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The macrophage in HIV-1 infection: From activation to deactivation?

  1. Author:
    Herbein, G.
    Varin, A.

  2. Author Address

    [Herbein, Georges; Varin, Audrey] Univ Franche Comte, CHU Besancon, Dept Virol, UPRES EA Pathogens & Inflammat 4266,IFR INSERM 13, F-25030 Besancon, France. [Varin, Audrey] NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.;Herbein, G, Univ Franche Comte, CHU Besancon, Dept Virol, UPRES EA Pathogens & Inflammat 4266,IFR INSERM 13, F-25030 Besancon, France.;georges.herbein@univ-fcomte.fr
    1. Year: 2010
    2. Date: Apr
  2. Journal: Retrovirology
    1. 7
    2. Pages: 15
  4. Type of Article: Review
  5. Article Number: 33
  6. ISSN: 1742-4690
  1. Abstract:

    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-gamma 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.

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External Sources

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  2. DOI: 10.1186/1742-4690-7-33
  3. View record in Web of Science®
  4. WOS: 000277408000001

Library Notes

  1. Fiscal Year: FY2009-2010
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