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

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, Alexander T. Phythian-Adams, Elisabeth Wachter, Lauren M. Webb, Tara E. Sutherland, Graham D. Thomas, John R. Grainger, Jim Selfridge, Andrew N. J. McKenzie, Judith E. Allen, Susanna C. Fagerholm, Rick M. Maizels, Alasdair C. Ivens, Adrian Bird and Andrew S. MacDonald ()
Additional contact information
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

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms7920

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