Prevention of Arthritis by Interleukin 10–producing B Cells

By C. Mauri, D. Gray, Naseem Mushtaq, M. Londei. Journal of Experimental Medicine, 2003

915 citations recorded by the source corpus.

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.

Subfields: Immunology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/72bc1a7ee68c8c2976c807640cee7db41f60ac9f

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In Immunology

1. C. Mauri
2. E. Rosser
3. Stephen Anderton
4. D. Gray

Citations in the corpus

• Regulation of IFN-γ Production by B Effector 1 Cells: Essential Roles for T-bet and the IFN-γ Receptor1 (2005, background): “Importantly, cytokine-producing B cells play a critical protective role in several autoimmune disease models, including inflammatory bowel disease (4), experimental autoimmune encephalomyelitis (6), and collagen-induced arthritis (5).”
• CD19(+)CD24(hi)CD38(hi) B cells exhibit regulatory capacity in healthy individuals but are functionally impaired in systemic Lupus Erythematosus patients. (2010, background): “In CIA, stimulation of B cells with an agonistic CD40 mAb gives rise to a population of B cells with potent suppres- sive capacity both in vivo and in vitro (Mauri et al., 2003).”
• Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression. (2008, background): “IL-10–produced by B cells can also down-regulate other autoimmune and inflammatory diseases such as collagen-induced arthritis, inflammatory bowel disease, and contact hypersensitivity (17, 41, 42).”
• B cell depletion therapy ameliorates autoimmune disease through ablation of IL-6–producing B cells (2012, background): “Thus, in addition to their documented regulatory capacity (Mauri et al., 2003; Mann et al., 2007; Fillatreau et al., 2008; Lampropoulou et al., 2008), B cells also promote the inflammatory response in EAE and MS (Anderton and Fillatreau, 2008; Lampropoulou et al., 2010).”
• Regulatory B cells: origin, phenotype, and function. (2015, background): “If unresolved, this inflammatory response causes injury to host tissues, which can lead to the development of a wide variety of immune-mediated pathologies (Medzhitov, 2008).”
• Distinct Effector Cytokine Profiles of Memory and Naive Human B Cell Subsets and Implication in Multiple Sclerosis (2007, result): “This concept is supported by our novel observation that B cells from MS patients exhibit a relative deficiency in their capacity to produce this down-regulatory cytokine, a finding that also extends results from recent animal model studies reporting that IL-10 produced by B cells can protect against”