B cells from glatiramer acetate-treated mice suppress experimental autoimmune encephalomyelitis

Mrinalini Kala, Susan N. Rhodes, Wen Hua Piao, Fu Dong Shi, Denise I. Campagnolo, Timothy L. Vollmer

Research output: Contribution to journalArticlepeer-review

84 Scopus citations


Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) thought to be primarily mediated by T cells. However, emerging evidence supports an important role for B cells in the pathogenesis and inhibition of MS. Glatiramer acetate (GA), a Food and Drug Administration-approved drug for the treatment of MS, has a good safety profile. But GA's mechanism of action in MS is still elusive. In this study, we showed that B cells from GA-treated mice increased production of IL-10 and reduced expression of co-stimulatory molecules viz.: CD80 and CD86. B cells from GA-treated mice also diminished proliferation of myelin oligodendrocyte glycoprotein (MOG35-55) specific T cells. Purified B cells transferred from GA-treated mice suppressed experimental autoimmune encephalomyelitis (EAE) in recipient mice compared with B cells transferred from mice treated with PBS or ovalbumin. The treatment effect of GA in EAE was abrogated in B cell-deficient mice. Transfer of B cells from GA-treated mice inhibited the proliferation of autoreactive T cells as well as the development of Th1 and Th17 cells but promoted IL-10 production in recipient mice. The number of peripheral CD11b+ macrophages in recipient mice also decreased after transfer of B cells from GA-treated mice; however, the number of dendritic cells and regulatory T cells remained unaltered. These results suggest that B cells are important to the protective effects of GA in EAE.

Original languageEnglish (US)
Pages (from-to)136-145
Number of pages10
JournalExperimental Neurology
Issue number1
StatePublished - Jan 2010
Externally publishedYes


  • B cells
  • Experimental autoimmune encephalomyelitis
  • Glatiramer acetate/Copaxone
  • Multiple sclerosis

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience


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