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Loss of IL-10 secretion by regulatory B lymphocytes in multiple sclerosis patients

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HAL Id: inserm-00643972

https://www.hal.inserm.fr/inserm-00643972

Submitted on 23 Nov 2011

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Loss of IL-10 secretion by regulatory B lymphocytes in

multiple sclerosis patients

Laure Michel, Nicolas Degauque, Alexandra Garcia, Marion Salou, Annie

Ngono, Jean-Paul Soulillou, David Laplaud, Sophie Brouard

To cite this version:

Laure Michel, Nicolas Degauque, Alexandra Garcia, Marion Salou, Annie Ngono, et al.. Loss of

IL-10 secretion by regulatory B lymphocytes in multiple sclerosis patients. 6th european workshop on

immune-mediated inflammatory diseases, Nice, France. pp.P25. �inserm-00643972�

(2)

P O S T E R P R E S E N T A T I O N

Open Access

Loss of IL-10 secretion by regulatory B

lymphocytes in multiple sclerosis patients

Laure Michel

1,2*

, Nicolas Degauque

1

, Alexandra Garcia

1

, Marion Salou

1

, Annie Elong Ngono

1

, Jean-Paul Soulillou

1

,

David Laplaud

1,2

, Sophie Brouard

1

From 6th European Workshop on Immune-Mediated Inflammatory Diseases

Nice, France. 23-25 November 2011

Background

Recently, an alternative role of B cells has emerged. Regu-latory B cells have been shown to down-regulate immune responses in mice and humans. These cells control disease progression in several models of human autoimmune diseases, including a model of Multiple Sclerosis (MS). Their regulatory function mostly relies on their capacity to produce IL-10.

Objectives

Our aim was to explore the frequency, the phenotype and the functional properties of regulatory B cells in MS patients compared to Healthy Volunteers (HV).

Methods

All patients suffered from MS and had not received immune drugs since at least 6 months. The frequency and the phenotype of B cell subsets have been analysed using different specific markers: CD19+CD27+memory B cells, CD19+CD38dimCD24dimmature naïve B cells and CD19+ CD24highCD38hightransitional B cells. Their capacity to secrete IL-10 was analysedin vitro 48 hours after stimula-tion by CD40 ligand and CpG ODN.

Results

Thirty-eight MS patients (mean age: 41.55±12.8 yrs) and 21 HV (mean age: 35.4±13.4 yrs, NS) have been included. The patients had different MS forms: Clini-cally Isolated Syndrome (n=5), Relapsing-Remitting (n=23), Secondary Progressive (n=4) and Primary Pro-gressive (n=6).

No significant difference was found for the frequency of the different B cell subsets in the different subgroups

of patients. Particularly, MS patients harbor the same number (in frequency and absolute value) of CD19+ CD24highCD38hightransitional B cells. However, the fre-quency of IL-10 secreting B cells was significantly decreased in MS patients (0.9±0.5%, n=9) compared to HV (2±0.95%, n=10, p<0.05, Mann Whitney test).

Discussion/perspectives

MS patients display the same frequency of CD19+ CD24highCD38hightransitional B cells, described as hav-ing regulatory properties. Nevertheless, B cells of MS patients present a significant decreased secretion of IL-10, supporting a defect in the B cells regulatory property. If confirmed, these results could have a considerable impact for the development of new therapeutic strategies.

Author details 1

INSERM U643, Nantes University, Nantes, France.2Neurology Dept., Nantes Hospital, Nantes, France.

Published: 23 November 2011

doi:10.1186/1479-5876-9-S2-P25

Cite this article as: Michel et al.: Loss of IL-10 secretion by regulatory B lymphocytes in multiple sclerosis patients. Journal of Translational Medicine 2011 9(Suppl 2):P25.

1INSERM U643, Nantes University, Nantes, France

Full list of author information is available at the end of the article Michel et al. Journal of Translational Medicine 2011, 9(Suppl 2):P25 http://www.translational-medicine.com/content/9/S2/P25

© 2011 Michel et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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