Abstract

When B cells react aggressively against self, the potential for pathology is extreme. It is therefore not surprising that B-cell depletion is seen as an attractive therapy in autoimmune diseases. However, B cells can also be essential for restraining unwanted autoaggressive T-cell responses. Recent advances have pointed to interleukin-10 (IL-10) production as a key component in B-cell-mediated immune regulation. In this Opinion article, we develop a hypothesis that triggering of Toll-like receptors controls the propensity of B cells for IL-10 production and immune suppression. According to this model, B cells can translate exposure to certain microbial infections into protection from chronic inflammatory diseases.

Author affiliations

1. Simon Fillatreau is at the Immune regulation group, Deutsches Rheuma-ForschungsZentrum, Charitéplatz 1, 10117 Berlin, Germany.
2. David Gray and Stephen M. Anderton are at the University of Edinburgh, Institute of Immunology and Infection Research, School of Biological Sciences, Kings Buildings, West Mains Road, Edinburgh EH9 3JT, UK.
3. Stephen M. Anderton is also at the University of Edinburgh, Centre for Inflammation Research, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.

Correspondence to: Stephen M. Anderton³ Email: steve.anderton@ed.ac.uk

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