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A dendritic cell-specific intercellular adhesion molecule 3- grabbing nonintegrin (DC-SIGN)-related protein is highly expressed on human liver sinusoidal endothelial cells and promotes HIV-1 infection

  1. Author:
    Bashirova, A. A.
    Geijtenbeek, T. B. H.
    van Duijnhoven, G. C. F.
    van Vliet, S. J.
    Eilering, J. B. G.
    Martin, M. P.
    Wu, L.
    Martin, T. D.
    Viebig, N.
    Knolle, P. A.
    KewalRamani, V. N.
    van Kooyk, Y.
    Carrington, M.

  2. Author Address

    NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, Sci Applicat Int Corp, POB B, Frederick, MD 21702 USA. Zentrum Mol Biol Heidelberg, ZMBH, D-69120 Heidelberg, Germany. Univ Nijmegen, Med Ctr St Radbound, Tumor Immunol Dept, NL-6525 EX Nijmegen, Netherlands. NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA. NCI, Lab Genomic Divers, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, Sci Applicat Int Corp, Frederick, MD 21702 USA. Carrington M NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, Sci Applicat Int Corp, POB B, Frederick, MD 21702 USA.
    1. Year: 2001
  2. Journal: Journal of Experimental Medicine
    1. 193
    2. 6
    3. Pages: 671-678
  4. Type of Article: Article
  1. Abstract:

    The discovery of dendritic cell (DC)-specific intercellular adhesion molecule (ICAM)-3-grabbing nonintegrin (DC-SIGN) as a DC-specific ICAM-3 binding receptor that enhances HIV-1 infection of T cells in trans has indicated a potentially important role for adhesion molecules in AIDS pathogenesis. A related molecule called DC-SIGNR exhibits 77% amino acid sequence identity with DC-SIGN. The DC-SIGN and DC-SIGNR genes map within a 30-kb region on chromosome 19p13.2-3. Their strong homology and close physical location indicate a recent duplication of the original gene. Messenger RNA and protein expression patterns demonstrate that the DC-SIGN-related, molecule is highly expressed on Liver sinusoidal cells and in the lymph node but not on DCs, ill contrast to DC-SIGN. Therefore, we suggest that a more appropriate name for the DC- SIGN-related molecule is L-SIGN, liver/lymph node-specific ICAM-3-grabbing nonintegrin. We show that in the liver, L-SIGN is expressed by sinusoidal endothelial cells. Functional studies indicate that L-SIGN behaves similarly to DC-SIGN in that it has a high affinity for ICAM-3, captures HIV-1 through gp120 binding, and enhances HIV-1 infection of T cells in trans. We propose that L-SIGN may play an important role in the interaction between liver sinusoidal endothelium and trafficking lymphocytes, as well as function in the pathogenesis of HIV-1.

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