Melanoma cell adhesion molecule identifies encephalitogenic T lymphocytes and promotes their recruitment to the central nervous system (original) (raw)

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11 Neuroimmunology Research Laboratory, Centre of Excellence in Neuromics, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montréal, Québec, H2L 2W5, Canada

22 Multiple Sclerosis Clinic, Department of Neurology, Université de Montréal, CHUM-Notre-Dame Hospital, Montréal, Québec, H2L 4M1, Canada

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Revision received:

29 May 2012

Published:

13 September 2012

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Catherine Larochelle, Romain Cayrol, Hania Kebir, Jorge Ivan Alvarez, Marc-André Lécuyer, Igal Ifergan, Émilie Viel, Lyne Bourbonnière, Diane Beauseigle, Simone Terouz, Lamia Hachehouche, Steve Gendron, Josée Poirier, Céline Jobin, Pierre Duquette, Ken Flanagan, Ted Yednock, Nathalie Arbour, Alexandre Prat, Melanoma cell adhesion molecule identifies encephalitogenic T lymphocytes and promotes their recruitment to the central nervous system, Brain, Volume 135, Issue 10, October 2012, Pages 2906–2924, https://doi.org/10.1093/brain/aws212
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Abstract

In multiple sclerosis, encephalitogenic CD4+ lymphocytes require adhesion molecules to accumulate into central nervous system inflammatory lesions. Using proteomic techniques, we identified expression of melanoma cell adhesion molecule (MCAM) on a subset of human effector memory CD4+ lymphocytes and on human blood–brain barrier endothelium. Herein, we demonstrate that MCAM is a stable surface marker that refines the identification of interleukin 17+, interleukin 22+, RAR-related orphan receptor γ and interleukin 23 receptor+ cells within the CD161+CCR6+ subset of memory CD4+ lymphocytes. We also show that MCAM+ lymphocytes express significantly more granulocyte/macrophage colony stimulating factor and granzyme B than MCAM− lymphocytes. Furthermore, the proportion of MCAM+ CD4+ lymphocytes is significantly increased in the blood and in the central nervous system of patients with multiple sclerosis and experimental autoimmune encephalomyelitis animals compared with healthy controls or other neurological diseases, and MCAM expression is upregulated at the blood–brain barrier within inflammatory lesions. Moreover, blockade of MCAM or depletion of MCAM+ CD4+ T lymphocytes both restrict the migration of TH17 lymphocytes across blood–brain barrier endothelial cells and decrease the severity of experimental autoimmune encephalomyelitis. Our findings indicate that MCAM could serve as a potential biomarker for multiple sclerosis and represents a valuable target for the treatment of neuroinflammatory conditions.

© The Author (2012). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com

Topic:

• cell adhesion molecules
• endothelial cells
• central nervous system
• granulocyte-macrophage colony-stimulating factor
• blood-brain barrier
• experimental autoimmune encephalomyelitis
• interleukin-17
• lymphocytes
• melanoma
• multiple sclerosis
• t-lymphocytes
• memory
• interleukin-22
• granzyme b

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