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Related Experiment Video

Updated: Dec 28, 2025

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c-Met is expressed by highly autoreactive encephalitogenic CD8+ cells.

Mahdia Benkhoucha1, Isis Senoner1, Patrice H Lalive2,3

  • 1Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.

Journal of Neuroinflammation
|February 21, 2020
PubMed
Summary

Hepatocyte growth factor (HGF) restrains cytotoxic CD8+ T cells expressing c-Met receptor in neuroinflammatory diseases. Targeting the HGF/c-Met pathway may modulate these T cells for treating central nervous system autoimmune conditions.

Keywords:
CD8+ T cellEAEHGFMSNeuroinflammationc-Met

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Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • CD8+ T lymphocytes are key players in neuroinflammatory diseases.
  • Understanding their function is vital for central nervous system autoimmune disease research.
  • A novel population of cytotoxic c-Met-expressing CD8+ T cells was identified.

Purpose of the Study:

  • To investigate the role of c-Met-expressing CD8+ T cells in a mouse model of experimental autoimmune encephalitis (EAE).
  • To explore the impact of hepatocyte growth factor (HGF) on these cells' function.

Main Methods:

  • Induction of EAE in mice using myelin oligodendrocyte glycoprotein peptide (MOG35-55).
  • Evaluation of inflammation, c-Met expression on CD8+ T cells via flow cytometry and immunofluorescence.
  • Analysis of molecular, cellular, and killing functions using PCR, ELISA, and cytotoxicity assays.

Main Results:

  • A subset of effector CD8+ T cells expressed c-Met (c-Met+CD8+) in the EAE model.
  • These cells recognized the MOG37-50 epitope and produced high levels of interferon-γ and granzyme B.
  • Hepatocyte growth factor (HGF) was found to directly inhibit the cytotoxic activity of c-Met+CD8+ T cells.

Conclusions:

  • The HGF/c-Met pathway plays a significant role in regulating CD8+ T cell responses in neuroinflammation.
  • This pathway presents a potential therapeutic target for modulating CD8+ T cell-mediated neuroinflammatory diseases.