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Updated: May 18, 2026

Flow Cytometric Analysis of Lymphocyte Infiltration in Central Nervous System during Experimental Autoimmune Encephalomyelitis
09:01

Flow Cytometric Analysis of Lymphocyte Infiltration in Central Nervous System during Experimental Autoimmune Encephalomyelitis

Published on: November 17, 2020

Melanoma cell adhesion molecule identifies encephalitogenic T lymphocytes and promotes their recruitment to the

Catherine Larochelle1, Romain Cayrol, Hania Kebir

  • 1Neuroimmunology Research Laboratory, Centre of Excellence in Neuromics, Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), Montréal, Québec, H2L 2W5, Canada.

Brain : a Journal of Neurology
|September 15, 2012
PubMed

Insights

Melanoma cell adhesion molecule (MCAM) is found on T cells that drive multiple sclerosis. Blocking MCAM reduces neuroinflammation and disease severity, suggesting MCAM as a therapeutic target.

Area of Science:

  • Neuroimmunology
  • Cellular and Molecular Immunology

Background:

  • Encephalitogenic CD4(+) lymphocytes use adhesion molecules to infiltrate the central nervous system in multiple sclerosis.
  • Melanoma cell adhesion molecule (MCAM) expression was identified on human effector memory CD4(+) lymphocytes and blood-brain barrier endothelium.

Purpose of the Study:

  • To investigate the role of MCAM in T cell migration and its potential as a biomarker and therapeutic target in multiple sclerosis.

Main Methods:

  • Proteomic techniques to identify MCAM expression.
  • Flow cytometry to characterize MCAM(+) CD4(+) T lymphocytes.
  • In vivo studies using experimental autoimmune encephalomyelitis (EAE) models.
  • In vitro assays to assess T cell migration across blood-brain barrier endothelium.

Main Results:

  • MCAM is a stable surface marker identifying specific subsets of memory CD4(+) T lymphocytes (interleukin-17+, interleukin-22+, RAR-related orphan receptor γ+, interleukin-23 receptor+).
  • MCAM(+) lymphocytes exhibit higher expression of granulocyte/macrophase colony-stimulating factor and granzyme B.
  • Increased proportion of MCAM(+) CD4(+) lymphocytes in multiple sclerosis patients and EAE animals; MCAM is upregulated at the blood-brain barrier in lesions.
  • MCAM blockade or MCAM(+) CD4(+) T cell depletion reduced T(H)17 cell migration and EAE severity.

Conclusions:

  • MCAM is a potential biomarker for multiple sclerosis.
  • MCAM represents a promising therapeutic target for neuroinflammatory conditions.
  • Targeting MCAM may inhibit T cell infiltration into the central nervous system and ameliorate disease.

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