• Open Access

Helminth-induced CD19+CD23hi B cells modulate experimental allergic and autoimmune inflammation

Authors

  • Mark S. Wilson,

    1. Centre for Immunity, Infection and Evolution, and Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK
    Current affiliation:
    1. Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MA 20892 USA
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  • Matthew D. Taylor,

    1. Centre for Immunity, Infection and Evolution, and Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK
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  • Mary T. O'Gorman,

    1. Centre for Immunity, Infection and Evolution, and Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK
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  • Adam Balic,

    1. Centre for Immunity, Infection and Evolution, and Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK
    Current affiliation:
    1. Surgical Research Laboratory, Murdoch Children's Research Institute, The Royal Children's Hospital, Parkville 3052, Australia
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  • Tom A. Barr,

    1. Centre for Immunity, Infection and Evolution, and Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK
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  • Kara Filbey,

    1. Centre for Immunity, Infection and Evolution, and Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK
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  • Stephen M. Anderton,

    1. Centre for Immunity, Infection and Evolution, and Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK
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  • Rick M. Maizels

    Corresponding author
    1. Centre for Immunity, Infection and Evolution, and Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK
    • Institute of Immunology and Infection Research, University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, UK Fax: +44-131-650-5450
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Abstract

Numerous population studies and experimental models suggest that helminth infections can ameliorate immuno-inflammatory disorders such as asthma and autoimmunity. Immunosuppressive cell populations associated with helminth infections include Treg and alternatively-activated macrophages. In previous studies, we showed that both CD4+CD25+ Treg, and CD4 MLN cells from Heligmosomoides polygyus-infected C57BL/6 mice were able to transfer protection against allergic airway inflammation to sensitized but uninfected animals. We now show that CD4CD19+ MLN B cells from infected, but not naïve, mice are able to transfer a down-modulatory effect on allergy, significantly suppressing airway eosinophilia, IL-5 secretion and pathology following allergen challenge. We further demonstrate that the same cell population can alleviate autoimmune-mediated inflammatory events in the CNS, when transferred to uninfected mice undergoing myelin oligodendrocyte glycoprotein(p35–55)-induced EAE. In both allergic and autoimmune models, reduction of disease was achieved with B cells from helminth-infected IL-10−/− donors, indicating that donor cell-derived IL-10 is not required. Phenotypically, MLN B cells from helminth-infected mice expressed uniformly high levels of CD23, with follicular (B2) cell surface markers. These data expand previous observations and highlight the broad regulatory environment that develops during helminth infections that can abate diverse inflammatory disorders in vivo.

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