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A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells

Author

Listed:
  • Peter C. Cook

    (Manchester Collaborative Centre for Inflammation Research, University of Manchester)

  • Heather Owen

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Aimée M. Deaton

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh)

  • Jessica G. Borger

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Sheila L. Brown

    (Manchester Collaborative Centre for Inflammation Research, University of Manchester)

  • Thomas Clouaire

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh)

  • Gareth-Rhys Jones

    (Manchester Collaborative Centre for Inflammation Research, University of Manchester)

  • Lucy H. Jones

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Rachel J. Lundie

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Angela K. Marley

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Vicky L. Morrison

    (Medical Research Institute, Ninewells Hospital and Medical School, University of Dundee)

  • Alexander T. Phythian-Adams

    (Manchester Collaborative Centre for Inflammation Research, University of Manchester)

  • Elisabeth Wachter

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh)

  • Lauren M. Webb

    (Manchester Collaborative Centre for Inflammation Research, University of Manchester)

  • Tara E. Sutherland

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Graham D. Thomas

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • John R. Grainger

    (Manchester Collaborative Centre for Inflammation Research, University of Manchester)

  • Jim Selfridge

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh)

  • Andrew N. J. McKenzie

    (Medical Research Council Laboratory of Molecular Biology)

  • Judith E. Allen

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Susanna C. Fagerholm

    (Medical Research Institute, Ninewells Hospital and Medical School, University of Dundee)

  • Rick M. Maizels

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Alasdair C. Ivens

    (Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh)

  • Adrian Bird

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh)

  • Andrew S. MacDonald

    (Manchester Collaborative Centre for Inflammation Research, University of Manchester)

Abstract

Dendritic cells (DCs) direct CD4+ T-cell differentiation into diverse helper (Th) subsets that are required for protection against varied infections. However, the mechanisms used by DCs to promote Th2 responses, which are important both for immunity to helminth infection and in allergic disease, are currently poorly understood. We demonstrate a key role for the protein methyl-CpG-binding domain-2 (Mbd2), which links DNA methylation to repressive chromatin structure, in regulating expression of a range of genes that are associated with optimal DC activation and function. In the absence of Mbd2, DCs display reduced phenotypic activation and a markedly impaired capacity to initiate Th2 immunity against helminths or allergens. These data identify an epigenetic mechanism that is central to the activation of CD4+ T-cell responses by DCs, particularly in Th2 settings, and reveal methyl-CpG-binding proteins and the genes under their control as possible therapeutic targets for type-2 inflammation.

Suggested Citation

  • Peter C. Cook & Heather Owen & Aimée M. Deaton & Jessica G. Borger & Sheila L. Brown & Thomas Clouaire & Gareth-Rhys Jones & Lucy H. Jones & Rachel J. Lundie & Angela K. Marley & Vicky L. Morrison & A, 2015. "A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells," Nature Communications, Nature, vol. 6(1), pages 1-11, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7920
    DOI: 10.1038/ncomms7920
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    Cited by:

    1. E. L. Houlder & A. H. Costain & I. Nambuya & S. L. Brown & J. P. R. Koopman & M. C. C. Langenberg & J. J. Janse & M. A. Hoogerwerf & A. J. L. Ridley & J. E. Forde-Thomas & S. A. P. Colombo & B. M. F. , 2023. "Pulmonary inflammation promoted by type-2 dendritic cells is a feature of human and murine schistosomiasis," Nature Communications, Nature, vol. 14(1), pages 1-12, December.

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