Antibody-independent B cell effector functions in relapsing remitting Multiple Sclerosis: Clues to increased inflammatory and reduced regulatory B cell capacity

Sara J. Ireland, Monica Blazek, Christopher T. Harp, Benjamin Greenberg, Elliot M. Frohman, Laurie S. Davis, Nancy L. Monson

Research output: Contribution to journalArticle

43 Scopus citations

Abstract

The pathogenic role for B cells in the context of relapsing remitting multiple sclerosis (MS) is incompletely defined. Although classically considered a T cell-mediated disease, B cell-depleting therapies showed efficacy in treating the clinical symptoms of RRMS without decreasing plasma cells or total immunoglobulin (Ig) levels. Here, we discuss the potential implications of antibody-independent B cell effector functions that could contribute to autoimmunity with particular focus on antigen presentation, cytokine secretion, and stimulation of T cell subsets. We highlight differences between memory and naïve B cells from MS patients such as our recent findings of hyper-proliferation from MS memory B cells in response to CD40 engagement. We discuss the implications of IL6 overproduction in contrast to limited IL10 production by B cells from MS patients and comment on the impact of these functions on yet unexplored aspects of B cells in autoimmune disease. Finally, we contextualize B cell effector functions with respect to current immunomodulatory therapies for MS and show that glatiramer acetate (GA) does not directly modulate B cell proliferation or cytokine secretion.

Original languageEnglish (US)
Pages (from-to)400-414
Number of pages15
JournalAutoimmunity
Volume45
Issue number5
DOIs
StatePublished - Aug 1 2012

Keywords

  • B cell APC function
  • B cell co-stimulation molecules
  • B cell cytokines
  • B cell proliferation
  • B-T interaction

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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