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B-cell-derived interleukin-10 in autoimmune disease: regulating the regulators

Nature Reviews Immunology volume 8, pages 486–487 (2008)Cite this article

The authors' work3, however, primarily highlights the role of memory B-cell IL-10 in downregulating the active inflammatory response in EAE (that is, disease remission), less so the role of B-cell IL-10 in the prevention of chronic inflammatory disease. Is it the authors' opinion that we largely rely on infectious agents to generate the regulatory B cells that contribute not only to recovery from exacerbation of autoimmune disease, but also to the maintenance of immune homeostasis and thus our ability to avoid the initial development of autoimmune disease?

As an alternative teleological explanation for these findings3, we suggest that TLR-induced immune downregulation by memory B-cell IL-10 evolved as a mechanism that limits otherwise adaptive pathogen-specific responses (TH1-cell and/or TH17-cell responses) from becoming overly aggressive. This would be expected to occur when memory B cells integrate sufficiently strong stimulatory signals, such as combined engagement of TLR, B-cell receptor (BCR) and CD40, during vigorous adaptive immune responses, such as pathogen-specific responses. IL-10 induced in these B cells could then contribute through a 'negative-feedback loop' to downregulate the local immune response, thereby limiting excessive self-tissue damage. The existence of such a mechanism as part of the normal resolution of pathogen-specific responses could also contribute to the remission from a dysregulated adaptive immune response, such as exacerbation of a TH1- or TH17-cell-driven autoimmune disease4.

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  1. Aja Rieger and Amit Bar-Or are at the Neuroimmunology Unit, Montreal Neurological Institute, 3801 University Street, Montreal, Quebec, H3A2B4 Canada.,

    Aja Rieger & Amit Bar-Or

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  1. Aja Rieger
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Rieger, A., Bar-Or, A. B-cell-derived interleukin-10 in autoimmune disease: regulating the regulators. Nat Rev Immunol 8, 486–487 (2008). https://doi.org/10.1038/nri2315-c1

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