Differential Susceptibility to Human Immunodeficiency Virus Type 1 Infection of Myeloid and Plasmacytoid Dendritic Cells

DOI Web Site 被引用文献3件
  • Anna Smed-Sörensen
    Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden
  • Karin Loré
    Immunology Laboratory
  • Jayanand Vasudevan
    Immunology Laboratory
  • Mark K. Louder
    BSL-3 Virology Laboratory, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland
  • Jan Andersson
    Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden
  • John R. Mascola
    BSL-3 Virology Laboratory, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland
  • Anna-Lena Spetz
    Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden
  • Richard A. Koup
    Immunology Laboratory

抄録

<jats:title>ABSTRACT</jats:title><jats:p>Human immunodeficiency virus type 1 (HIV-1) infection of dendritic cells (DCs) plays an important role in HIV-1 transmission and pathogenesis. Here, we studied the susceptibility of ex vivo-isolated CD11c<jats:sup>+</jats:sup>myeloid DCs (MDCs) and CD123<jats:sup>+</jats:sup>plasmacytoid DCs (PDCs) to HIV-1 infection and the function of these cells early after infection. Both DC subsets were susceptible to CCR5- and CXCR4-using HIV-1 isolates (BaL and IIIB, respectively). However, MDCs were more susceptible to HIV-1<jats:sub>BaL</jats:sub>infection than donor-matched PDCs. In addition, HIV-1<jats:sub>BaL</jats:sub>infected MDCs more efficiently than HIV-1<jats:sub>IIIB</jats:sub>, whereas PDCs were equally susceptible to both isolates. While exposure to HIV-1 alone resulted in only weak maturation of DCs, Toll-like receptor 7/8 ligation induced full maturation in both infected and uninfected DCs. Maturation did not increase HIV-1 replication in infected DCs, and infected DCs retained their ability to produce tumor necrosis factor alpha after stimulation. Both HIV-1 isolates induced alpha interferon production exclusively in PDCs, irrespective of productive infection. In conclusion, PDCs and MDCs were susceptible to HIV-1 infection, but neither displayed functional defects as a consequence of infection. The difference in susceptibility of PDCs and MDCs to HIV-1 may have implications for HIV-1 transmission and DC-mediated transfer of HIV-1 to T cells.</jats:p>

収録刊行物

  • Journal of Virology

    Journal of Virology 79 (14), 8861-8869, 2005-07

    American Society for Microbiology

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