Skip Navigation



International Immunology Advance Access published online on August 16, 2007

International Immunology, doi:10.1093/intimm/dxm071
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
19/8/1011    most recent
dxm071v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Lebbink, R. J.
Right arrow Articles by Meyaard, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lebbink, R. J.
Right arrow Articles by Meyaard, L.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

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

Robert Jan Lebbink1, Talitha de Ruiter1, Guido J. A. Kaptijn1, Dominique G. Bihan2, Christine A. Jansen1, Peter J. Lenting3 and Linde Meyaard1

1 Department of Immunology, University Medical Center Utrecht, Lundlaan 6, 3584 EA Utrecht, The Netherlands
2 Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK
3 Thrombosis and Haemostasis Laboratory, Department of Clinical Chemistry and Haematology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands

Correspondence to: Correspondence to: L. Meyaard; E-mail: l.meyaard{at}umcutrecht.nl

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.

Keywords: CD305, immune receptor, ITIM, regulation


Transmitting editor: I. Pecht

Received 29 September 2006, accepted 30 May 2007.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Leukoc. Biol.Home page
L. Meyaard
The inhibitory collagen receptor LAIR-1 (CD305)
J. Leukoc. Biol., April 1, 2008; 83(4): 799 - 803.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
A. D. Konitsiotis, N. Raynal, D. Bihan, E. Hohenester, R. W. Farndale, and B. Leitinger
Characterization of High Affinity Binding Motifs for the Discoidin Domain Receptor DDR2 in Collagen
J. Biol. Chem., March 14, 2008; 283(11): 6861 - 6868.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.