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HIV-1 infection-induced apoptotic microparticles inhibit human DCs via CD44.

Authors
  • Frleta, Davor
  • Ochoa, Carolyn E
  • Kramer, Holger B
  • Khan, Shaukat Ali
  • Stacey, Andrea R
  • Borrow, Persephone
  • Kessler, Benedikt M
  • Haynes, Barton F
  • Bhardwaj, Nina
Type
Published Article
Journal
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Publication Date
Dec 01, 2012
Volume
122
Issue
12
Pages
4685–4697
Identifiers
DOI: 10.1172/JCI64439
PMID: 23160198
Source
Medline
License
Unknown

Abstract

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.

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