Regulatory B Cells Induce Formation of IL-10-Expressing T Cells in Mice with Autoimmune Neuroinflammation

• Authors: Andrea Pennati, University of Wisconsin; Spencer Ng, Emory University; Yuanqiang Wu, Emory University; Jordan R. Murphy, Emory University; Jiusheng Deng, Emory University; Srikant Rangaraju, Emory University; Seneshaw Asress, Emory University; Jennifer Blanchfield, Emory University; Brian Evavold, Emory University; Jacques Galipeau, Emory University
• Journal Title: Journal of Neuroscience Nursing
• Volume: Volume 36, Number 50
• Publisher: Lippincott, Williams & Wilkins | 2016-12-14, Pages 12598-12610
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.1523/JNEUROSCI.1994-16.2016
• Subjects: Health Sciences, Immunology; Biology, Neuroscience
• Keywords: Science & Technology; Life Sciences & Biomedicine; Neurosciences; Neurosciences & Neurology; B10 CELLS; MULTIPLE-SCLEROSIS; IL-10; DISEASE; ARTHRITIS; IMMUNITY; ENCEPHALOMYELITIS; INFLAMMATION; EXPANSION; LIGAND

Abstract

Although B cells are traditionally known for their role in propagating proinflammatory immune responses, their immunosuppressive effects have only recently begun to be appreciated. How these regulatory B cells (Bregs) suppress the immune response remains to be worked out in detail. In this article, we show that Bregs can induce the formation of conventional FoxP3+regulatory T cells (Tregs), as well as a more recently described CD49b+CD223+ regulatory T-cell subset, known as type 1 regulatory T cells (Tr1s). When Bregs are transferred into mice with experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, they home to the spleen and mesenteric lymph nodes, leading to an expansion of Tregs and Tr1 in vivo. Tregs and Tr1s are also found in greater proportions in the CNS of mice with EAE treated with Bregs and are correlated with the remission of symptoms. The discovery that Bregs induce the formation of regulatory T-cell subsets in vivo may herald their use as immunosuppressive agents in adoptive cellular therapies for autoimmune pathologies.