Accelerated central nervous system autoimmunity in BAFF-receptor-deficient mice

J Neurol Sci. 2011 Jul 15;306(1-2):9-15. doi: 10.1016/j.jns.2011.04.008. Epub 2011 May 6.

Abstract

B cell activating factor (BAFF) is critical for B cell survival, a function that is mediated by BAFF receptor, (BAFF-R). The role of BAFF (or BAFF-R) in the multiple sclerosis model, experimental autoimmune encephalomyelitis (EAE), was examined using BAFF-R-deficient mice. BAFF-R deficiency resulted in paradoxically increased severity of EAE induced by myelin-oligodendrocyte glycoprotein (MOG) peptide 35-55. Inflammatory foci in BAFF-R-deficient mice comprised increased numbers of activated macrophages expressing BAFF and correlated with increased BAFF secretion. Thus, BAFF-R may be important in EAE pathogenesis, possibly by influencing macrophage function through a mechanism that involves modulation of BAFF expression.

Publication types

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

MeSH terms

  • Animals
  • Autoimmunity*
  • B-Cell Activation Factor Receptor / deficiency
  • Central Nervous System / immunology*
  • Central Nervous System / pathology
  • Central Nervous System / physiopathology
  • Cytokines / metabolism
  • Disease Models, Animal
  • Encephalomyelitis, Autoimmune, Experimental / immunology
  • Encephalomyelitis, Autoimmune, Experimental / pathology*
  • Enzyme-Linked Immunosorbent Assay / methods
  • Glycoproteins / adverse effects
  • Lymphocytes / metabolism
  • Macrophages / metabolism
  • Macrophages / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myelin-Oligodendrocyte Glycoprotein
  • Peptide Fragments / adverse effects
  • Spleen / pathology
  • Statistics, Nonparametric

Substances

  • B-Cell Activation Factor Receptor
  • Cytokines
  • Glycoproteins
  • Myelin-Oligodendrocyte Glycoprotein
  • Peptide Fragments
  • Tnfrsf13c protein, mouse
  • myelin oligodendrocyte glycoprotein (35-55)