Toll-like receptor (TLR)7 and TLR9 agonists enhance interferon (IFN) beta-1a's immunoregulatory effects on B cells in patients with relapsing-remitting multiple sclerosis (RRMS).

Journal Article (Journal Article)

We report that B cells from patients with RRMS have decreased endogenous IFN-β secretion and deficient IFN receptor (IFNAR)1/2 and TLR7 gene expression in comparison to healthy controls (HCs), which may contribute to disregulation of cytokine secretion by B cells. We propose that TLR7 and TLR9 stimulation with loxorubin (LOX) and CpG, in combination with exogenous IFN-β may effectively reconstitute endogenous IFN-β production deficit and induce the secretion of immunoregulatory cytokines by B cells. Both LOX/IFN-β and CpG/IFN-β in-vitro treatments of B cells from RRMS patients induced higher endogenous IFN-β gene expression in comparison to the exogenous IFN-β alone. CpG/IFN-β combination induced higher secretion of IL-10, TGF-β, and IL-27 in comparison to stimulation with IFN-β. Our study provides a basis for future clinical studies employing IFN-β and TLR7/9 agonists, which may enhance the resolution of the inflammatory response in RRMS.

Full Text

Duke Authors

Cited Authors

  • Tao, Y; Zhang, X; Markovic-Plese, S

Published Date

  • September 15, 2016

Published In

Volume / Issue

  • 298 /

Start / End Page

  • 181 - 188

PubMed ID

  • 27609294

Electronic International Standard Serial Number (EISSN)

  • 1872-8421

Digital Object Identifier (DOI)

  • 10.1016/j.jneuroim.2016.07.019


  • eng

Conference Location

  • Netherlands