ACKR1 favors transcellular over paracellular T‐cell diapedesis across the blood‐brain barrier in neuroinflammation in vitro

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  • Luca Marchetti
    Theodor Kocher Institute University of Bern Bern Switzerland
  • David Francisco
    Interfaculty Bioinformatics Unit and Swiss Institute of Bioinformatics University of Bern Bern Switzerland
  • Sasha Soldati
    Theodor Kocher Institute University of Bern Bern Switzerland
  • Neda Haghayegh Jahromi
    Theodor Kocher Institute University of Bern Bern Switzerland
  • Sara Barcos
    Theodor Kocher Institute University of Bern Bern Switzerland
  • Isabelle Gruber
    Theodor Kocher Institute University of Bern Bern Switzerland
  • Javier R. Pareja
    Theodor Kocher Institute University of Bern Bern Switzerland
  • Aude Thiriot
    Department of Immunology and Center for Immune Imaging Harvard Medical School Boston Massachusetts USA
  • Ulrich von Andrian
    Department of Immunology and Center for Immune Imaging Harvard Medical School Boston Massachusetts USA
  • Urban Deutsch
    Theodor Kocher Institute University of Bern Bern Switzerland
  • Ruth Lyck
    Theodor Kocher Institute University of Bern Bern Switzerland
  • Rémy Bruggmann
    Interfaculty Bioinformatics Unit and Swiss Institute of Bioinformatics University of Bern Bern Switzerland
  • Britta Engelhardt
    Theodor Kocher Institute University of Bern Bern Switzerland

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<jats:title>Abstract</jats:title><jats:p>The migration of CD4<jats:sup>+</jats:sup> effector/memory T cells across the blood–brain barrier (BBB) is a critical step in MS or its animal model, EAE. T‐cell diapedesis across the BBB can occur paracellular, via the complex BBB tight junctions or transcellular via a pore through the brain endothelial cell body. Making use of primary mouse brain microvascular endothelial cells (pMBMECs) as in vitro model of the BBB, we here directly compared the transcriptome profile of pMBMECs favoring transcellular or paracellular T‐cell diapedesis by RNA sequencing (RNA‐seq). We identified the atypical chemokine receptor 1 (<jats:italic>Ackr1</jats:italic>) as one of the main candidate genes upregulated in pMBMECs favoring transcellular T‐cell diapedesis. We confirmed upregulation of ACKR1 protein in pMBMECs promoting transcellular T‐cell diapedesis and in venular endothelial cells in the CNS during EAE. Lack of endothelial ACKR1 reduced transcellular T‐cell diapedesis across pMBMECs under physiological flow in vitro. Combining our previous observation that endothelial ACKR1 contributes to EAE pathogenesis by shuttling chemokines across the BBB, the present data support that ACKR1 mediated chemokine shuttling enhances transcellular T‐cell diapedesis across the BBB during autoimmune neuroinflammation.</jats:p>

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