Intercellular Adhesion Molecule-1 (ICAM-1) and ICAM-2 Differentially Contribute to Peripheral Activation and CNS Entry of Autoaggressive Th1 and Th17 Cells in Experimental Autoimmune Encephalomyelitis.
- Haghayegh Jahromi N Theodor Kocher Institute, University of Bern, Bern, Switzerland.
- Marchetti L Theodor Kocher Institute, University of Bern, Bern, Switzerland.
- Moalli F Theodor Kocher Institute, University of Bern, Bern, Switzerland.
- Duc D Laboratories of Neuroimmunology, Division of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Epalinges, Switzerland.
- Basso C Institute for Research in Biomedicine, Università della Svizzera Italiana, Bellinzona, Switzerland.
- Tardent H Theodor Kocher Institute, University of Bern, Bern, Switzerland.
- Kaba E Theodor Kocher Institute, University of Bern, Bern, Switzerland.
- Deutsch U Theodor Kocher Institute, University of Bern, Bern, Switzerland.
- Pot C Laboratories of Neuroimmunology, Division of Neurology and Neuroscience Research Center, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Epalinges, Switzerland.
- Sallusto F Institute for Research in Biomedicine, Università della Svizzera Italiana, Bellinzona, Switzerland.
- Stein JV Theodor Kocher Institute, University of Bern, Bern, Switzerland.
- Engelhardt B Theodor Kocher Institute, University of Bern, Bern, Switzerland.
- 2020-01-30
Published in:
- Frontiers in immunology. - 2019
ICAM-1
ICAM-2
T cell activation
Th1 cells
Th17 cells
blood-brain barrier
dendritic cells
experimental autoimmune encephalomyelitis
Animals
Antigens, CD
Blood-Brain Barrier
Cell Adhesion Molecules
Encephalomyelitis, Autoimmune, Experimental
Intercellular Adhesion Molecule-1
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Th1 Cells
Th17 Cells
Transendothelial and Transepithelial Migration
English
In experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), myelin-specific T cells are activated in the periphery and differentiate in T helper (Th) 1 and Th17 effector cells, which cross the blood-brain barrier (BBB) to reach the central nervous system (CNS), where they induce neuroinflammation. Here, we explored the role of intercellular adhesion molecule-1 (ICAM-1) and ICAM-2 in the activation of naïve myelin-specific T cells and in the subsequent migration of differentiated encephalitogenic Th1 and Th17 cells across the BBB in vitro and in vivo. While on antigen-presenting cells ICAM-1, but not ICAM-2 was required for the activation of naïve CD4+ T cells, endothelial ICAM-1 and ICAM-2 mediated both Th1 and Th17 cell migration across the BBB. ICAM-1/-2-deficient mice developed ameliorated typical and atypical EAE transferred by encephalitogenic Th1 and Th17 cells, respectively. Our study underscores important yet cell-specific contributions for ICAM-1 and ICAM-2 in EAE pathogenesis.
- Language
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- English
- Open access status
- gold
- Identifiers
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- DOI 10.3389/fimmu.2019.03056
- PMID 31993059
- Persistent URL
- https://folia.unifr.ch/global/documents/111500
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