Multiple sclerosis

J Clin Invest. 2012 Apr;122(4):1180-8. doi: 10.1172/JCI58649. Epub 2012 Apr 2.


Multiple sclerosis (MS) is a multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual. While the formation and persistence of meningeal lymphoid follicles suggest persistence of antigens to drive the continuing inflammatory and humoral response, the identity of an antigen or infectious agent leading to the oligoclonal expansion of B and T cells is unknown. In this review we examine new paradigms for understanding the immunopathology of MS, present recent data defining the common genetic variants underlying disease susceptibility, and explore how improved understanding of immune pathway disruption can inform MS prognosis and treatment decisions.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Alleles
  • Autoantigens / immunology
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / immunology
  • B-Lymphocyte Subsets / immunology
  • Costimulatory and Inhibitory T-Cell Receptors / genetics
  • Costimulatory and Inhibitory T-Cell Receptors / immunology
  • Cytokines / genetics
  • Cytokines / metabolism
  • Forecasting
  • Forkhead Transcription Factors / deficiency
  • Forkhead Transcription Factors / physiology
  • Genetic Predisposition to Disease
  • Genome-Wide Association Study
  • Humans
  • Lymphocyte Activation
  • Meninges / immunology
  • Models, Immunological
  • Multiple Sclerosis / genetics
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / pathology
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocytes, Regulatory / immunology


  • Autoantigens
  • Costimulatory and Inhibitory T-Cell Receptors
  • Cytokines
  • FOXP3 protein, human
  • Forkhead Transcription Factors