JAML mediates monocyte and CD8 T cell migration across the brain endothelium
Leukocyte transmigration into the central nervous system promotes multiple sclerosis pathogenesis, yet ambiguity remains regarding the mechanisms controlling the migration of distinct immune cell subsets. Using in vitro, ex vivo and postmortem human materials, we identified a significant upregulatio...
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John Wiley and Sons Inc.
2015
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Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4693623/ |
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pubmed-46936232016-01-05 JAML mediates monocyte and CD8 T cell migration across the brain endothelium Alvarez, Jorge Iván Kébir, Hania Cheslow, Lara Chabarati, Marc Larochelle, Catherine Prat, Alexandre Brief Communications Leukocyte transmigration into the central nervous system promotes multiple sclerosis pathogenesis, yet ambiguity remains regarding the mechanisms controlling the migration of distinct immune cell subsets. Using in vitro, ex vivo and postmortem human materials, we identified a significant upregulation of junctional adhesion molecule‐like expression at the blood–brain barrier, monocytes, and CD8 T cells of multiple sclerosis patients. We also detected junctional adhesion molecule‐like+ trans‐migratory cups when monocytes/CD8 T cells adhered to the blood–brain barrier, however, their migratory capacity was significantly compromised when junctional adhesion molecule‐like was blocked. These findings highlight a novel role for junctional adhesion molecule‐like in leukocyte transmigration and its potential as a promising therapeutic target. John Wiley and Sons Inc. 2015-09-29 /pmc/articles/PMC4693623/ /pubmed/26734656 http://dx.doi.org/10.1002/acn3.255 Text en © 2015 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Alvarez, Jorge Iván Kébir, Hania Cheslow, Lara Chabarati, Marc Larochelle, Catherine Prat, Alexandre |
spellingShingle |
Alvarez, Jorge Iván Kébir, Hania Cheslow, Lara Chabarati, Marc Larochelle, Catherine Prat, Alexandre JAML mediates monocyte and CD8 T cell migration across the brain endothelium |
author_facet |
Alvarez, Jorge Iván Kébir, Hania Cheslow, Lara Chabarati, Marc Larochelle, Catherine Prat, Alexandre |
author_sort |
Alvarez, Jorge Iván |
title |
JAML mediates monocyte and CD8 T cell migration across the brain endothelium |
title_short |
JAML mediates monocyte and CD8 T cell migration across the brain endothelium |
title_full |
JAML mediates monocyte and CD8 T cell migration across the brain endothelium |
title_fullStr |
JAML mediates monocyte and CD8 T cell migration across the brain endothelium |
title_full_unstemmed |
JAML mediates monocyte and CD8 T cell migration across the brain endothelium |
title_sort |
jaml mediates monocyte and cd8 t cell migration across the brain endothelium |
description |
Leukocyte transmigration into the central nervous system promotes multiple sclerosis pathogenesis, yet ambiguity remains regarding the mechanisms controlling the migration of distinct immune cell subsets. Using in vitro, ex vivo and postmortem human materials, we identified a significant upregulation of junctional adhesion molecule‐like expression at the blood–brain barrier, monocytes, and CD8 T cells of multiple sclerosis patients. We also detected junctional adhesion molecule‐like+ trans‐migratory cups when monocytes/CD8 T cells adhered to the blood–brain barrier, however, their migratory capacity was significantly compromised when junctional adhesion molecule‐like was blocked. These findings highlight a novel role for junctional adhesion molecule‐like in leukocyte transmigration and its potential as a promising therapeutic target. |
publisher |
John Wiley and Sons Inc. |
publishDate |
2015 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4693623/ |
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1613517464436473856 |