scholarly journals Dendritic Cell-Specific Intercellular Adhesion Molecule 3-Grabbing Nonintegrin/CD209 Is Abundant on Macrophages in the Normal Human Lymph Node and Is Not Required for Dendritic Cell Stimulation of the Mixed Leukocyte Reaction

2005 ◽  
Vol 175 (7) ◽  
pp. 4265-4273 ◽  
Author(s):  
Angela Granelli-Piperno ◽  
Alla Pritsker ◽  
Maggi Pack ◽  
Irina Shimeliovich ◽  
Jean-Francois Arrighi ◽  
...  
Keyword(s):  
Lymph Node ◽  
Dendritic Cell ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Mixed Leukocyte Reaction ◽  
Cell Stimulation ◽  
Human Lymph Node ◽  
Normal Human ◽  
Stimulation Of

scholarly journals 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

2001 ◽  
Vol 193 (6) ◽  
pp. 671-678 ◽  
Author(s):  
Arman A. Bashirova ◽  
Teunis B.H. Geijtenbeek ◽  
Gerard C.F. van Duijnhoven ◽  
Sandra J. van Vliet ◽  
Jeroen B.G. Eilering ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Lymph Node ◽  
Dendritic Cell ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Related Molecule ◽  
In Trans ◽  
Hiv 1

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.

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