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

Susan S. Kim, David P Richman, Scott S. Zamvil, Mark A. Agius

Research output: Contribution to journalArticle

20 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)9-15
Number of pages7
JournalJournal of the Neurological Sciences
Volume306
Issue number1-2
DOIs
StatePublished - Jul 15 2011

Keywords

  • B-cell activating factor
  • BAFF-receptor
  • Central nervous system inflammation
  • Experimental autoimmune encephalomyelitis
  • Macrophages
  • Multiple sclerosis
  • T-cells

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

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