Retinoic acid enhances the levels of IL-10 in TLR-stimulated B cells from patients with relapsing-remitting multiple sclerosis

Agnete Bratsberg Eriksen; Tone Berge; Marte Wendel Gustavsen; Ingvild Sørum Leikfoss; Steffan Daniel Bos; Anne Spurkland; Hanne F Harbo; Heidi Kiil Blomhoff

doi:10.1016/j.jneuroim.2014.11.019

Retinoic acid enhances the levels of IL-10 in TLR-stimulated B cells from patients with relapsing-remitting multiple sclerosis

J Neuroimmunol. 2015 Jan 15:278:11-8. doi: 10.1016/j.jneuroim.2014.11.019. Epub 2014 Nov 24.

Authors

Agnete Bratsberg Eriksen¹, Tone Berge², Marte Wendel Gustavsen³, Ingvild Sørum Leikfoss³, Steffan Daniel Bos³, Anne Spurkland⁴, Hanne F Harbo³, Heidi Kiil Blomhoff⁵

Affiliations

¹ Department of Biochemistry, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
² Department of Neurology, Oslo University Hospital, Ullevål, Oslo, Norway.
³ Department of Neurology, Oslo University Hospital, Ullevål, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
⁴ Department of Anatomy, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
⁵ Department of Biochemistry, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. Electronic address: h.k.blomhoff@medisin.uio.no.

PMID: 25595247
DOI: 10.1016/j.jneuroim.2014.11.019

Abstract

We have explored the beneficial effects of retinoic acid (RA) on B cells from multiple sclerosis (MS) patients. When co-stimulated via the toll-like receptors (TLRs) TLR9 and RP105, MS B cells secreted less of the anti-inflammatory cytokine interleukin 10 (IL-10) compared to B cells from healthy controls. Importantly, RA enhanced the secretion of IL-10 by MS-derived B cells without affecting the levels of the pro-inflammatory cytokine TNF-α. RA revealed the same ability to induce IL-10 as did interferon-β-1b (IFN-β-1b), and B-cells from patients treated with glatiramer acetate or IFN-β-1b still displayed the beneficial effects of RA on the IL-10/TNF-α ratio.

Keywords: B cells; IL-10; Multiple sclerosis; Retinoic acid; TLR; TNF-α.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adult
Aged
Antigens, CD / pharmacology*
Antigens, CD19 / metabolism
B-Lymphocytes / drug effects*
B-Lymphocytes / metabolism
Cell Proliferation / drug effects
Cells, Cultured
Female
Glatiramer Acetate
Humans
Immunosuppressive Agents / pharmacology
Interleukin-10 / metabolism*
Keratolytic Agents / pharmacology*
Middle Aged
Multiple Sclerosis, Relapsing-Remitting / pathology*
Peptides / pharmacology
Toll-Like Receptor 9 / metabolism
Tretinoin / pharmacology*
Tumor Necrosis Factor-alpha / metabolism

Substances

Antigens, CD
Antigens, CD19
CD180 protein, human
Immunosuppressive Agents
Keratolytic Agents
Peptides
Toll-Like Receptor 9
Tumor Necrosis Factor-alpha
Interleukin-10
Tretinoin
Glatiramer Acetate