
JAML mediates monocyte and CD8 T cell migration across the brain endothelium
Author(s) -
Alvarez Jorge Iván,
Kébir Hania,
Cheslow Lara,
Chabarati Marc,
Larochelle Catherine,
Prat Alexandre
Publication year - 2015
Publication title -
annals of clinical and translational neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.824
H-Index - 42
ISSN - 2328-9503
DOI - 10.1002/acn3.255
Subject(s) - cell adhesion molecule , microbiology and biotechnology , medicine , monocyte , cd8 , adhesion , multiple sclerosis , endothelium , immunology , blood–brain barrier , cell adhesion , immune system , in vitro , pathogenesis , ex vivo , central nervous system , biology , chemistry , biochemistry , endocrinology , organic chemistry
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.