2007
DOI: 10.1016/j.humimm.2006.10.014
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Nucleoside Reverse Transcriptase Inhibitors Are Able and Protease Inhibitors Unable to Induce the Tolerogenic Molecule HLA-G1 on Monocytes From HIV-1 Infected Patients

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Cited by 13 publications
(15 citation statements)
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“…Some reports, indeed, demonstrate that both the monocyte/macrophage lineage is less permeable to antiretroviral compounds 43 and some anti-reverse transcriptase compounds increase membrane expression of HLA-G, which negatively modulates killing of virus-infected cells by NK cells and autologous CD4þ T-cell activation. 44 Moreover, the linear correlation between PBLs and monocyte DNA load observed in our study may also suggest a relationship between these reservoirs and a possible infectious refeeding between them, in accord with Garbuglia and coworkers, 14 even though other papers indicated that some patients could harbor genetically distinct HIV-1 quasispecies. 45 In conclusion, this report indicates that effective longterm HAART significantly decreases the HIV-1 DNA load both in PBLs and monocytes in HAART-treated patients compared to naïve individuals.…”
Section: Discussionsupporting
confidence: 90%
“…Some reports, indeed, demonstrate that both the monocyte/macrophage lineage is less permeable to antiretroviral compounds 43 and some anti-reverse transcriptase compounds increase membrane expression of HLA-G, which negatively modulates killing of virus-infected cells by NK cells and autologous CD4þ T-cell activation. 44 Moreover, the linear correlation between PBLs and monocyte DNA load observed in our study may also suggest a relationship between these reservoirs and a possible infectious refeeding between them, in accord with Garbuglia and coworkers, 14 even though other papers indicated that some patients could harbor genetically distinct HIV-1 quasispecies. 45 In conclusion, this report indicates that effective longterm HAART significantly decreases the HIV-1 DNA load both in PBLs and monocytes in HAART-treated patients compared to naïve individuals.…”
Section: Discussionsupporting
confidence: 90%
“…Our results are also consistent with the reported increase in the membrane expression of HLA-G molecules on monocytes, T lymphocytes, and CD8 ϩ regulatory T cells obtained from HIVpositive patients [18,33] as well as with recently published data reporting that monocytes and dendritic cells from HIV-1-infected subjects secrete increased amounts of intracellularly stored HLA-G molecules that interfere, by interaction with the HLA class I receptor LILRB2 (ILT4), with myeloid dendritic cells function inhibiting their antigen-presenting properties and enhancing their secretion of proinflammatory cytokines [34]. By contrast, the decrease of sHLA-G serum levels that we have detected after HAART seems in disagreement with the finding that HLA-G expression on monocytes is increased by antiretroviral drugs [35], especially by nucleoside reverse transcriptase inhibitors [36]. However, in these reports, it has not been evaluated whether the increased HLA-G membrane expression may induce an augmented shedding of soluble HLA-G molecules.…”
Section: Discussioncontrasting
confidence: 85%
“…Most HIV-1-infected individuals analyzed in the latter study were on antiretroviral therapy, whereas all of our study participants were naive to treatment. Antiretroviral therapy can induce surface expression of HLA-G on blood peripheral monocytes from HIV-1-infected patients [17,18]. Hence, the relatively high blood levels of HLA-G observed in the French subjects could be caused by antiretroviral therapy and not HIV-1 infection per se.…”
Section: Discussionmentioning
confidence: 96%