Loading…

Mouse leukocyte-associated Ig-like receptor-1 (mLAIR-1) functions as an inhibitory collagen-binding receptor on immune cells

Leukocyte-associated Ig-like receptor-1 (LAIR-1) is a cell-surface molecule that functions as an inhibitory receptor on various immune cells. We developed mAbs to study the expression of mouse leukocyte-associated Ig-like receptor-1 (mLAIR-1) on primary immune cells and established that it is expres...

Full description

Saved in:
Bibliographic Details
Published in:International immunology 2007-08, Vol.19 (8), p.1011-1019
Main Authors: Lebbink, Robert Jan, de Ruiter, Talitha, Kaptijn, Guido J. A., Bihan, Dominique G., Jansen, Christine A., Lenting, Peter J., Meyaard, Linde
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Leukocyte-associated Ig-like receptor-1 (LAIR-1) is a cell-surface molecule that functions as an inhibitory receptor on various immune cells. We developed mAbs to study the expression of mouse leukocyte-associated Ig-like receptor-1 (mLAIR-1) on primary immune cells and established that it is expressed on the majority of cells of the immune system, including T cells, NK cells, monocytes and dendritic cells. Furthermore, mLAIR-1 is inducibly expressed on blood granulocytes in vivo and is differentially expressed upon T cell activation in vitro. Unexpectedly, mLAIR-1 was not expressed on splenic and blood B220+ B cells. Similar to its human homolog, mLAIR-1 interacted with high affinity with a wide range of collagen molecules. Furthermore, mLAIR-1 specifically interacted in a hydroxyproline-dependent manner with synthetic collagen Gly-Pro-Hyp peptides. We show, for the first time, that mLAIR-1 cross-linking with its ligands inhibits CD3-induced T cell stimulation in vitro. Given the similarities between the mouse and human receptors, mLAIR-1 may serve as a good model to assess the role of the LAIR-1 receptors in regulation of immune responses.
ISSN:0953-8178
1460-2377
DOI:10.1093/intimm/dxm071