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

doi:10.1084/jem.193.6.671

Published online 12 March 2001.

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© The Rockefeller University Press, 0022-1007/2001/3/671/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 6, March 19, 2001 671-678

Original Article

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

Arman A. Bashirova^a, Teunis B.H. Geijtenbeek^d, Gerard C.F. van Duijnhoven^d, Sandra J. van Vliet^d, Jeroen B.G. Eilering^d, Maureen P. Martin^b, Li Wu^c, Thomas D. Martin^c, Nicola Viebig^e, Percy A. Knolle^e, Vineet N. KewalRamani^c, Yvette van Kooyk^d, and Mary Carrington^b
^a Laboratory of Genomic Diversity, Science Applications International Corporation-Frederick,
^b Intramural Research Support Program, Science Applications International Corporation-Frederick,
^c HIV Drug Resistance Program, National Cancer Institute-Frederick, Frederick, Maryland 21702
^d Tumor Immunology Department, University Medical Center St. Radbound, Nijmegen 6525 EX, The Netherlands
^e Zentrum für Moleculare Biologie Heidelberg (ZMBH), D-69120 Heidelberg, Germany

Correspondence to: Mary Carrington, P.O. Box B, NCI-FCRDC, Frederick, MD 21702. Tel:301-846-1390 Fax:301-846-1909 E-mail:carringt{at}mail.ncifcrf.gov.

The discovery of dendritic cell (DC)-specific intercellularadhesion molecule (ICAM)-3–grabbing nonintegrin (DC-SIGN)as a DC-specific ICAM-3 binding receptor that enhances HIV-1infection of T cells in trans has indicated a potentially importantrole for adhesion molecules in AIDS pathogenesis. A relatedmolecule called DC-SIGNR exhibits 77% amino acid sequence identitywith DC-SIGN. The DC-SIGN and DC-SIGNR genes map within a 30-kbregion on chromosome 19p13.2-3. Their strong homology and closephysical location indicate a recent duplication of the originalgene. Messenger RNA and protein expression patterns demonstratethat the DC-SIGN–related molecule is highly expressedon liver sinusoidal cells and in the lymph node but not on DCs,in contrast to DC-SIGN. Therefore, we suggest that a more appropriatename for the DC-SIGN–related molecule is L-SIGN, liver/lymphnode–specific ICAM-3–grabbing nonintegrin. We showthat in the liver, L-SIGN is expressed by sinusoidal endothelialcells. Functional studies indicate that L-SIGN behaves similarlyto DC-SIGN in that it has a high affinity for ICAM-3, capturesHIV-1 through gp120 binding, and enhances HIV-1 infection ofT cells in trans. We propose that L-SIGN may play an importantrole in the interaction between liver sinusoidal endotheliumand trafficking lymphocytes, as well as function in the pathogenesisof HIV-1.

Key Words: L-SIGN, adhesion receptor, chromosome 19p13.2-3, ICAM-3, HIV-1gp120

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