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Prevention of Arthritis by Interleukin 10–producing B Cells

Open access
Mauri, Claudia, Gray, David, Mushtaq, Naseem, Londei, Marco·2003·The Journal of Experimental Medicine

Abstract

In this study we have shown that activation of arthritogenic splenocytes with antigen and agonistic anti-CD40 gives raise to a B cell population that produce high levels of interleukin (IL)-10 and low levels of interferon (IFN)-γ. Transfer of these B cells into DBA/1-TcR-β-Tg mice, immunized with bovine collagen (CII) emulsified in complete Freund's adjuvant inhibited T helper type 1 differentiation, prevented arthritis development, and was also effective in ameliorating established disease. IL-10 is essential for the regulatory function of this subset of B cells, as the B cells population isolated from IL-10 knockout mice failed to mediate this protective function. Furthermore, B cells isolated from arthritogenic splenocytes treated in vitro with anti–IL-10/anti–IL-10R were unable to protect recipient mice from developing arthritis. Our results suggest a new role of a subset of B cells in controlling T cell differentiation and autoimmune disorders.

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Metadata

Authors
Mauri, C., Gray, D., Mushtaq, N., & Londei, M.
Venue
The Journal of Experimental Medicine
Published
2003-02-10
Volume
197
Issue
4
Pages
489-501
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2168516002
Cited by
860
References
3
FWCI
6.55
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Prevention of Arthritis by Interleukin 10–producing B Cells. https://app.cochat.ai/papers/10.1084/jem.20021293
The paper
Mauri, C., Gray, D., Mushtaq, N., & Londei, M. (2003). Prevention of Arthritis by Interleukin 10–producing B Cells. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20021293

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.