Treatment of ongoing autoimmune encephalomyelitis with activated B-cell progenitors maturing into regulatory B cells

Sarantis Korniotis, Christophe Gras, Hélène Letscher, Ruddy Montandon, Jérôme Mégret, Stefanie Siegert, Sophie Ezine, Padraic G. Fallon, Sanjiv A. Luther, Simon Fillatreau and Flora Zavala ()
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Sarantis Korniotis: Institut Necker Enfants Malades, Immunology, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431
Christophe Gras: Institut Necker Enfants Malades, Immunology, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431
Hélène Letscher: Institut Necker Enfants Malades, Immunology, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431
Ruddy Montandon: Institut Necker Enfants Malades, Immunology, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431
Jérôme Mégret: Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine Site Necker, 14 rue Maria Helena Vieira da Silva, CS 61431
Stefanie Siegert: University of Lausanne
Sophie Ezine: Institut Necker Enfants Malades, Immunology, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431
Padraic G. Fallon: Trinity Biomedical Sciences Institute, Trinity College Dublin
Sanjiv A. Luther: University of Lausanne
Simon Fillatreau: Institut Necker Enfants Malades, Immunology, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431
Flora Zavala: Institut Necker Enfants Malades, Immunology, Inserm U1151, CNRS UMR 8253, 14 rue Maria Helena Vieira da Silva, CS 61431

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract The influence of signals perceived by immature B cells during their development in bone marrow on their subsequent functions as mature cells are poorly defined. Here, we show that bone marrow cells transiently stimulated in vivo or in vitro through the Toll-like receptor 9 generate proB cells (CpG-proBs) that interrupt experimental autoimmune encephalomyelitis (EAE) when transferred at the onset of clinical symptoms. Protection requires differentiation of CpG-proBs into mature B cells that home to reactive lymph nodes, where they trap T cells by releasing the CCR7 ligand, CCL19, and to inflamed central nervous system, where they locally limit immunopathogenesis through interleukin-10 production, thereby cooperatively inhibiting ongoing EAE. These data demonstrate that a transient inflammation at the environment, where proB cells develop, is sufficient to confer regulatory functions onto their mature B-cell progeny. In addition, these properties of CpG-proBs open interesting perspectives for cell therapy of autoimmune diseases.

Date: 2016
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DOI: 10.1038/ncomms12134

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