Eriksen Agnete Bratsberg, Berge Tone, Gustavsen Marte Wendel, Leikfoss Ingvild Sørum, Bos Steffan Daniel, Spurkland Anne, Harbo Hanne F, Blomhoff Heidi Kiil
Department of Biochemistry, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Department of Neurology, Oslo University Hospital, Ullevål, Oslo, Norway.
J Neuroimmunol. 2015 Jan 15;278:11-8. doi: 10.1016/j.jneuroim.2014.11.019. Epub 2014 Nov 24.
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.
我们探究了维甲酸（RA）对多发性硬化症（MS）患者B细胞的有益作用。当通过Toll样受体（TLR）TLR9和RP105进行共刺激时，与健康对照者的B细胞相比，MS患者的B细胞分泌的抗炎细胞因子白细胞介素10（IL-10）较少。重要的是，RA增强了源自MS的B细胞分泌IL-10的能力，而不影响促炎细胞因子肿瘤坏死因子-α（TNF-α）的水平。RA诱导IL-10的能力与干扰素-β-1b（IFN-β-1b）相同，并且接受醋酸格拉替雷或IFN-β-1b治疗的患者的B细胞仍表现出RA对IL-10/TNF-α比值的有益影响。
