HIV-1 infection-induced apoptotic microparticles inhibit human DCs via CD44.
Acute HIV-1 infection results in dysregulated immunity, which contributes to poor control of viral infection. DCs are key regulators of both adaptive and innate immune responses needed for controlling HIV-1, and we surmised that factors elicited during acute HIV-1 infection might impede DC function. We derived immature DCs from healthy donor peripheral blood monocytes and treated them with plasma from uninfected control donors and donors with acute HIV-1 infections. We found that the plasma from patients with HIV specifically inhibited DC function. This suppression was mediated by elevated apoptotic microparticles derived from dying cells during acute HIV-1 infection. Apoptotic microparticles bound to and inhibited DCs through the hyaluronate receptor CD44. These data suggest that targeting this CD44-mediated inhibition by apoptotic microparticles could be a novel strategy to potentiate DC activation of HIV-specific immunity.
Duke Scholars
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Related Subject Headings
- Viremia
- Toll-Like Receptors
- Immunology
- Immunity, Innate
- Hyaluronan Receptors
- Humans
- HIV-1
- HIV Infections
- Dendritic Cells
- Cell-Derived Microparticles
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Viremia
- Toll-Like Receptors
- Immunology
- Immunity, Innate
- Hyaluronan Receptors
- Humans
- HIV-1
- HIV Infections
- Dendritic Cells
- Cell-Derived Microparticles