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

Author:

Bashirova Arman A.1,Geijtenbeek Teunis B.H.2,van Duijnhoven Gerard C.F.2,van Vliet Sandra J.2,Eilering Jeroen B.G.2,Martin Maureen P.3,Wu Li4,Martin Thomas D.4,Viebig Nicola5,Knolle Percy A.5,KewalRamani Vineet N.4,van Kooyk Yvette2,Carrington Mary3

Affiliation:

1. Laboratory of Genomic Diversity, Science Applications International Corporation-Frederick,

2. Tumor Immunology Department, University Medical Center St. Radbound, Nijmegen 6525 EX, The Netherlands

3. Intramural Research Support Program, Science Applications International Corporation-Frederick,

4. HIV Drug Resistance Program, National Cancer Institute-Frederick, Frederick, Maryland 21702

5. Zentrum für Moleculare Biologie Heidelberg (ZMBH), D-69120 Heidelberg, Germany

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, in 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.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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