Publication

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

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Last modified
  • 03/03/2025
Type of Material
Authors
    Andrea Pennati, University of WisconsinSpencer Ng, Emory UniversityYuanqiang Wu, Emory UniversityJordan R. Murphy, Emory UniversityJiusheng Deng, Emory UniversitySrikant Rangaraju, Emory UniversitySeneshaw Asress, Emory UniversityJennifer Blanchfield, Emory UniversityBrian Evavold, Emory UniversityJacques Galipeau, Emory University
Language
  • English
Date
  • 2016-12-14
Publisher
  • Lippincott, Williams & Wilkins
Publication Version
Copyright Statement
  • © 2016 the authors.
License
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 0888-0395
Volume
  • 36
Issue
  • 50
Start Page
  • 12598
End Page
  • 12610
Grant/Funding Information
  • National Multiple Sclerosis Society Grant FG1963A1/1 was awarded to J.L.B.
  • This work was supported by National Institutes of Health Grant R01-AI-093881.
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.
Author Notes
  • Correspondence should be addressed to Dr. Jacques Galipeau, 1111 Highland Avenue, 3009 Wisconsin Institute for Medical Research, Madison, WI 53792., jgalipeau@wisc.edu
Keywords
Research Categories
  • Biology, Neuroscience
  • Health Sciences, Immunology

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