Update on inflammation, neurodegeneration, and immunoregulation in multiple sclerosis: Therapeutic implications

Jeffrey L. Bennett, Olaf Stüve

Research output: Contribution to journalReview articlepeer-review

70 Scopus citations

Abstract

Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system of uncertain etiology. There is consensus that a dysregulated immune system plays a critical role in the pathogenesis of MS; therefore, we aim to summarize current hypotheses concerning the complex cellular and molecular interactions involved in the immunopathology of MS. Although CD4+ T lymphocytes have long been implicated in the immunopathology of MS, the role of other T-cell subtypes has been recognized. CD4+ and CD8+ cells have been isolated from different locations within MS lesions and γ/δ T cells have been isolated from early MS lesions. The prevalent dogma has been that CD4 + TH1 cells release cytokines and mediators of inflammation that may cause tissue damage, although CD4+ T H2 cells may be involved in modulation of these effects. Recent evidence, however, suggests that additional T-cell subsets play a prominent role in MS immunopathology: TH17 cells, CD8+ effector T cells, and CD4+ CD25+ regulatory T cells. In addition, laboratory and clinical data are accumulating on the prominent role of B lymphocytes and antigen-presenting cells in MS pathogenesis. On the basis of these observations, new therapeutic approaches for MS will need to focus on resetting multiple components of the immune system.

Original languageEnglish (US)
Pages (from-to)121-132
Number of pages12
JournalClinical Neuropharmacology
Volume32
Issue number3
DOIs
StatePublished - May 1 2009

Keywords

  • Alemtuzumab
  • Cladribine
  • Cytokines
  • Fingolimod
  • Immunopathophysiology
  • Rituximab
  • T cells
  • T17 cells

ASJC Scopus subject areas

  • Pharmacology
  • Clinical Neurology
  • Pharmacology (medical)

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