Journal
BLOOD
Volume 120, Issue 11, Pages 2259-2268Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2012-03-418681
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Funding
- Inserm
- Centre National de la Recherche Scientifique
- Universite Paris Descartes
- Universite Paris-Diderot
- ANRS
- Sidaction
- Inserm Direction de l'hospitalisation et de l'organisation des soins, Ministere de la Sante et des Sports
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HIV infects activated CD4(+) T cells and induces their depletion. Progressive HIV infection leading to AIDS is fueled by chronic immune hyperactivation, mediated by inflammatory cytokines like TNF alpha. This has been related to intestinal epithelial damage and microbial LPS translocation into the circulation. Using 11-color flow cytometry, cell sorting, and cell culture, we investigated the numbers and TNF alpha production of fully defined circulating dendritic cell and monocyte populations during HIV-1 infection. In 15 viremic, untreated patients, compared with 8 treated, virologically suppressed patients or to 13 healthy blood donors, circulating CD141 (BDCA-3)(+) and CD1c (BDCA-1)(+) dendritic cell counts were reduced. Conversely, CD14(+)CD16(++) monocyte counts were increased, particularly those expressing M-DC8, while classical CD14(++)CD16(-)M-DC8(-) monocyte numbers were unchanged. Blood mononuclear cells from viremic patients produced more TNF alpha in response to LPS than those from virologically suppressed patients. M-DC8(+) monocytes were mostly responsible for this overproduction. Moreover, M-DC8(+) monocytes differentiated in vitro from classical monocytes using M-CSF and GM-CSF, which is increased in viremic patient's plasma. This M-DC8(+) monocyte population, which is involved in the pathogenesis of chronic inflammatory diseases like Crohn disease, might thus be considered as a major actor in the immune hyperactivation fueling HIV infection progression. (Blood. 2012;120(11):2259-2268)
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