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JAM-L–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation
Junctional adhesion molecules (JAMs) are endothelial and epithelial adhesion molecules involved in the recruitment of circulating leukocytes to inflammatory sites. We show here that JAM-L, a protein related to the JAM family, is restricted to leukocytes and promotes their adhesion to endothelial cel...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600739/ https://www.ncbi.nlm.nih.gov/pubmed/19064666 http://dx.doi.org/10.1083/jcb.200805061 |
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author | Luissint, Anny-Claude Lutz, Pierre G. Calderwood, David A. Couraud, Pierre-Olivier Bourdoulous, Sandrine |
author_facet | Luissint, Anny-Claude Lutz, Pierre G. Calderwood, David A. Couraud, Pierre-Olivier Bourdoulous, Sandrine |
author_sort | Luissint, Anny-Claude |
collection | PubMed |
description | Junctional adhesion molecules (JAMs) are endothelial and epithelial adhesion molecules involved in the recruitment of circulating leukocytes to inflammatory sites. We show here that JAM-L, a protein related to the JAM family, is restricted to leukocytes and promotes their adhesion to endothelial cells. Cis dimerization of JAM-L is required to engage in heterophilic interactions with its cognate counter-receptor CAR (coxsackie and adenovirus receptor). Interestingly, JAM-L expressed on neutrophils binds CAR independently of integrin activation. However, on resting monocytes and T lymphocytes, which express the integrin VLA-4, JAM-L molecules engage in complexes with VLA-4 and mainly accumulate in their monomeric form. Integrin activation is required for the dissociation of JAM-L–VLA-4 complexes and the accumulation of functional JAM-L dimers, which indicates that the leukocyte integrin VLA-4 controls JAM-L function in cis by controlling its dimerization state. This provides a mechanism through which VLA-4 and JAM-L functions are coordinately regulated, allowing JAM-L to strengthen integrin-dependent adhesion of leukocytes to endothelial cells. |
format | Text |
id | pubmed-2600739 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-26007392009-06-15 JAM-L–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation Luissint, Anny-Claude Lutz, Pierre G. Calderwood, David A. Couraud, Pierre-Olivier Bourdoulous, Sandrine J Cell Biol Research Articles Junctional adhesion molecules (JAMs) are endothelial and epithelial adhesion molecules involved in the recruitment of circulating leukocytes to inflammatory sites. We show here that JAM-L, a protein related to the JAM family, is restricted to leukocytes and promotes their adhesion to endothelial cells. Cis dimerization of JAM-L is required to engage in heterophilic interactions with its cognate counter-receptor CAR (coxsackie and adenovirus receptor). Interestingly, JAM-L expressed on neutrophils binds CAR independently of integrin activation. However, on resting monocytes and T lymphocytes, which express the integrin VLA-4, JAM-L molecules engage in complexes with VLA-4 and mainly accumulate in their monomeric form. Integrin activation is required for the dissociation of JAM-L–VLA-4 complexes and the accumulation of functional JAM-L dimers, which indicates that the leukocyte integrin VLA-4 controls JAM-L function in cis by controlling its dimerization state. This provides a mechanism through which VLA-4 and JAM-L functions are coordinately regulated, allowing JAM-L to strengthen integrin-dependent adhesion of leukocytes to endothelial cells. The Rockefeller University Press 2008-12-15 /pmc/articles/PMC2600739/ /pubmed/19064666 http://dx.doi.org/10.1083/jcb.200805061 Text en © 2008 Luissint et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Research Articles Luissint, Anny-Claude Lutz, Pierre G. Calderwood, David A. Couraud, Pierre-Olivier Bourdoulous, Sandrine JAM-L–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation |
title | JAM-L–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation |
title_full | JAM-L–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation |
title_fullStr | JAM-L–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation |
title_full_unstemmed | JAM-L–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation |
title_short | JAM-L–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation |
title_sort | jam-l–mediated leukocyte adhesion to endothelial cells is regulated in cis by α4β1 integrin activation |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600739/ https://www.ncbi.nlm.nih.gov/pubmed/19064666 http://dx.doi.org/10.1083/jcb.200805061 |
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