B-cells and humoral immunity in multiple sclerosis. Implications for therapy

Immunol Res. 2008;40(3):224-34. doi: 10.1007/s12026-007-8009-6.

Abstract

B-cells and humoral immunity have been implicated in the pathogenesis of multiple sclerosis. The most common pattern of demyelinating pathology in multiple sclerosis is associated with the deposition of antibodies and the activation of complement, as well as T-cells and macrophages. Plasmapheresis has been found to be an efficient therapeutic approach in patients with this type of pathological lesion. Recent data have indicated that autoantibodies and complement C5b-9 may be involved in lesion formation and might also be beneficial for lesion repair. Thus, the role played by B-cells and humoral immunity is rather complex, and new strategies for targeting B-cell responses are continuing to emerge.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Antibodies, Monoclonal / therapeutic use
  • Antibodies, Monoclonal, Murine-Derived
  • Antibody Formation*
  • Autoantibodies / blood*
  • Autoantibodies / immunology
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism
  • Central Nervous System / immunology
  • Complement Membrane Attack Complex / immunology
  • Complement Membrane Attack Complex / metabolism*
  • Complement System Proteins / immunology
  • Complement System Proteins / metabolism*
  • Humans
  • Immunologic Factors / therapeutic use
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / therapy*
  • Myelin Sheath / immunology
  • Rituximab

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Murine-Derived
  • Autoantibodies
  • Complement Membrane Attack Complex
  • Immunologic Factors
  • Rituximab
  • Complement System Proteins