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Monocyte and Myeloid Dendritic Cell Activation Occurs Throughout HIV Type 2 Infection, an Attenuated Form of HIV Disease
Monocyte and Myeloid Dendritic Cell Activation Occurs Throughout HIV Type 2 Infection, an Attenuated Form of HIV Disease
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Monocyte and Myeloid Dendritic Cell Activation Occurs Throughout HIV Type 2 Infection, an Attenuated Form of HIV Disease
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Monocyte and Myeloid Dendritic Cell Activation Occurs Throughout HIV Type 2 Infection, an Attenuated Form of HIV Disease
Monocyte and Myeloid Dendritic Cell Activation Occurs Throughout HIV Type 2 Infection, an Attenuated Form of HIV Disease

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Monocyte and Myeloid Dendritic Cell Activation Occurs Throughout HIV Type 2 Infection, an Attenuated Form of HIV Disease
Monocyte and Myeloid Dendritic Cell Activation Occurs Throughout HIV Type 2 Infection, an Attenuated Form of HIV Disease
Journal Article

Monocyte and Myeloid Dendritic Cell Activation Occurs Throughout HIV Type 2 Infection, an Attenuated Form of HIV Disease

2013
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Overview
Monocytes and myeloid dendritic cells (mDCs) are important orchestrators of innate and human immunodeficiency virus (HIV)—specific immune responses and of the generalized inflammation that characterizes AIDS progression. To our knowledge, we are the first to investigate monocyte and mDC imbalances in HIV type 2 (HIV-2)—positive patients, who typically feature reduced viremia and slow disease progression despite the recognized ability of HIV-2 to establish viral reservoirs and overcome host restriction factors in myeloid cells. We found a heightened state of monocyte and mDC activation throughout HIV-2 infection (characterized by CD14 bright CD16 + expansion, as well as increased levels of soluble CD14, HLA-DR, and CD86), together with progressive mDC depletion. Importantly, HIV-2—positive patients also featured overexpression of the inhibitory molecule PD-L1 on monocytes and mDCs, which may act by limiting the production of proinflammatory molecules. These data, from patients with a naturally occurring form of attenuated HIV disease, challenge current paradigms regarding the role of monocytes in HIV/AIDS and open new perspectives regarding potential strategies to modulate inflammatory states.

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