Multiple sclerosis and optic neuritis: CCR5 and CXCR3 expressing T cells are augmented in blood and cerebrospinal

Natalia Teleshova1, Mikhail Pashenkov, Yu-Min Huang

  • 1Department of Neurology, Karolinska Institutet, Huddinge University Hospital, 14186 Stockholm, Sweden.

Journal of Neurology
|July 12, 2002
PubMed

Insights

Chemokine receptors CCR5 and CXCR3 are elevated in T cells of untreated multiple sclerosis (MS) patients, suggesting a role in central nervous system (CNS) invasion. Interferon-beta treatment may reduce this expression.

Area of Science:

  • Neuroimmunology
  • Molecular immunology
  • Cellular immunology

Background:

  • Chemokines are implicated in T-cell recruitment to the central nervous system (CNS) in multiple sclerosis (MS).
  • Understanding chemokine receptor expression is crucial for elucidating T-cell migration in MS pathogenesis.

Purpose of the Study:

  • To investigate the expression of Th1-related chemokine receptors CCR5 and CXCR3 in patients with MS.
  • To compare receptor expression in MS patients with healthy controls (HC) and other non-inflammatory neurological disease (OND) patients.
  • To assess the impact of interferon-beta (IFN-beta) treatment and optic neuritis (ON) on chemokine receptor expression.

Main Methods:

  • Flow cytometry was used to quantify T cells expressing CCR5 and CXCR3.
  • Analysis was performed on blood samples from MS patients, HC, and OND patients.
  • Cerebrospinal fluid (CSF) samples were analyzed from MS and OND patients.

Main Results:

  • Untreated MS patients showed higher percentages of CCR5 and CXCR3 expressing T cells in blood compared to HC.
  • Elevated CCR5 and CXCR3 expressing T cells were observed in CSF of MS patients versus OND patients.
  • MS patients undergoing IFN-beta treatment did not exhibit these elevated receptor percentages.
  • Patients with optic neuritis (ON) had increased CXCR3+ T cells in blood and CCR5+ T cells in CSF.

Conclusions:

  • Elevated CCR5 and CXCR3 expression on T cells may facilitate their migration into the CNS in MS.
  • IFN-beta treatment might exert a therapeutic effect by inhibiting chemokine receptor expression.
  • Chemokine receptor expression patterns in ON suggest early involvement in MS pathogenesis.