• Open Access

TLR-mediated stimulation of APC: Distinct cytokine responses of B cells and dendritic cells

Authors

  • Tom A. Barr Dr.,

    Corresponding author
    1. Institute of Immunology and Infection Research, School of Biological Science, University of Edinburgh, Edinburgh, UK
    • Institute of Immunology and Infection Research, University of Edinburgh, Ashworth Laboratories, King's Buildings, West Mains Road, Edinburgh EH9 3JT, UK, Fax: +44-131-6507322
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  • Sheila Brown,

    1. Institute of Immunology and Infection Research, School of Biological Science, University of Edinburgh, Edinburgh, UK
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  • Gemma Ryan,

    1. Institute of Immunology and Infection Research, School of Biological Science, University of Edinburgh, Edinburgh, UK
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  • Jiexin Zhao,

    1. Institute of Immunology and Infection Research, School of Biological Science, University of Edinburgh, Edinburgh, UK
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  • David Gray

    1. Institute of Immunology and Infection Research, School of Biological Science, University of Edinburgh, Edinburgh, UK
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Abstract

In addition to their role in humoral immunity, B lymphocytes are important antigen-presenting cells (APC). In the same way as other APC, B cells make cytokines upon activation and have the potential to modulate T cell responses. In this study, we investigated which mouse B cell subsets are the most potent cytokine producers, and examined the role of Toll-like receptors (TLR) in the control of secretion of IL-6, IL-10, IL-12 and IFN-γ by B cells. Production of some cytokines was restricted to particular subsets. Marginal zone and B1 cells were the predominant source of B cell IL-10 in the spleen. Conversely, follicular B cells were found to express IFN-γ mRNA directly ex vivo. The nature of the activating stimulus dramatically influenced the cytokine made by B cells. Thus, in response to combined TLR stimulation, or via phorbol esters, IFN-γ was secreted. IL-10 was elicited by T-dependent activation or stimulation through TLR2, 4 or 9. This pattern of cytokine expression contrasts with that elicited from dendritic cells. QRT-PCR array data indicate that this may be due to differential expression of TLR signalling molecules, effectors and adaptors. Our data highlight the potentially unique nature of immune modulation when B cells act as APC.

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