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No lack of regulatory B cells in patients with Multiple Sclerosis


Recent data support a prominent role for B cells in MS physiopathology. Recently it has emerged that subsets of B cells secreting IL-10 negatively regulate disease symptoms in Experimental Autoimmune Encephalomyelitis (EAE). However, the involvement of such regulatory B cells in MS remains unclear.


We aimed to study the frequency, phenotype and function of regulatory B cells in MS patients as compared to Healthy Volunteers (HV).


Sixty-three untreated MS patients and 58 HV were included in this study. IL-10 secretion by B cells and phenotype of IL-10+ B cells were studied after 5h (B10 cells) and 48h of stimulation (B10pro cells) by CD40L and ODN. Coculture assays with prestimulated B cells and responding CD4+CD25- T cells were performed for 3 days.


No significant difference was found either for IL-10 secretion ability of B cells after 5h or 48h of stimulation. The analysis of B10pro cells phenotype revealed mainly a memory phenotype in MS and HV, even if both naïve and immature subsets were also able to secrete IL-10. Prestimulated B cells from MS inhibited CD4+CD25- T cell proliferation in the same manner than HV by a contact dependent mechanism, independently of IL-10 and TGF-β secretion.


Altogether, our data show that regulatory B cells have a conserved frequency, phenotype and function in the blood of patients with MS suggesting that B cells do not contribute to the physiopathology of the disease.


This work was funded by ARSEP.

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David-Axel Laplaud and Sophie Brouard contributed equally to this work.

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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Michel, L., Chesneau, M., Manceau, P. et al. No lack of regulatory B cells in patients with Multiple Sclerosis. J Transl Med 10 (Suppl 3), O4 (2012).

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