Dual role of ALCAM in neuroinflammation and blood–brain barrier homeostasis

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  • Marc-André Lécuyer
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Olivia Saint-Laurent
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Lyne Bourbonnière
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Sandra Larouche
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Catherine Larochelle
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Laure Michel
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Marc Charabati
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Michael Abadier
    Theodor Kocher Institute, University of Bern, 3012 Bern, Switzerland;
  • Stephanie Zandee
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Neda Haghayegh Jahromi
    Theodor Kocher Institute, University of Bern, 3012 Bern, Switzerland;
  • Elizabeth Gowing
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Camille Pittet
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;
  • Ruth Lyck
    Theodor Kocher Institute, University of Bern, 3012 Bern, Switzerland;
  • Britta Engelhardt
    Theodor Kocher Institute, University of Bern, 3012 Bern, Switzerland;
  • Alexandre Prat
    Neuroimmunology Research Laboratory, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, Canada H2X 0A9;

Description

<jats:title>Significance</jats:title> <jats:p>Multiple sclerosis (MS) is an inflammatory disorder characterized by multifocal lesions in the central nervous system. These lesions are caused by infiltrating leukocytes that take advantage and/or actively participate in the disruption of the blood–brain barrier (BBB). In this study, the specific role of the adhesion molecule ALCAM (activated leukocyte cell adhesion molecule) present on BBB endothelial cells was assessed. We demonstrated that ALCAM knockout mice develop a more severe experimental autoimmune encephalomyelitis, the mouse model of MS, due to an increased permeability of the BBB. This phenotypic change is caused by a dysregulation of junctional molecules with which ALCAM indirectly binds, suggesting that in addition to its role in leukocyte transmigration, ALCAM regulates and maintains tight junction stability by acting as an adaptor molecule.</jats:p>

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