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

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells. / Cook, Peter C; Owen, Heather; Deaton, Aimée M et al.
In: Nature Communications, Vol. 6, 6920, 24.04.2015.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Cook, PC, Owen, H, Deaton, AM, Borger, JG, Brown, SL, Clouaire, T, Jones, G-R, Jones, LH, Lundie, RJ, Marley, AK, Morrison, VL, Phythian-Adams, AT, Wachter, E, Webb, LM, Sutherland, TE, Thomas, GD, Grainger, JR, Selfridge, J, McKenzie, ANJ, Allen, JE, Fagerholm, SC, Maizels, RM, Ivens, AC, Bird, A & MacDonald, AS 2015, 'A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells', Nature Communications, vol. 6, 6920. https://doi.org/10.1038/ncomms7920

APA

Cook, P. C., Owen, H., Deaton, A. M., Borger, J. G., Brown, S. L., Clouaire, T., Jones, G-R., Jones, L. H., Lundie, R. J., Marley, A. K., Morrison, V. L., Phythian-Adams, A. T., Wachter, E., Webb, L. M., Sutherland, T. E., Thomas, G. D., Grainger, J. R., Selfridge, J., McKenzie, A. N. J., ... MacDonald, A. S. (2015). A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells. Nature Communications, 6, Article 6920. https://doi.org/10.1038/ncomms7920

Vancouver

Cook PC, Owen H, Deaton AM, Borger JG, Brown SL, Clouaire T et al. A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells. Nature Communications. 2015 Apr 24;6:6920. doi: 10.1038/ncomms7920

Author

Cook, Peter C ; Owen, Heather ; Deaton, Aimée M et al. / A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells. In: Nature Communications. 2015 ; Vol. 6.

Bibtex

@article{255b33ed1e7f4769b9a8bbb9dfa93b46,
title = "A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells",
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. ",
keywords = "Allergens, Animals, CD4-Positive T-Lymphocytes, Cell Polarity, Chromatin Immunoprecipitation, DNA Methylation, DNA-Binding Proteins, Dendritic Cells, Enzyme-Linked Immunosorbent Assay, Epigenesis, Genetic, Flow Cytometry, Gene Expression Regulation, Hypersensitivity, Lymphocyte Activation, Mice, Mice, Knockout, Pyroglyphidae, RNA, Messenger, Reverse Transcriptase Polymerase Chain Reaction, Schistosoma mansoni, Schistosomiasis mansoni, Th2 Cells, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "Cook, {Peter C} and Heather Owen and Deaton, {Aim{\'e}e M} and Borger, {Jessica G} and Brown, {Sheila L} and Thomas Clouaire and Gareth-Rhys Jones and Jones, {Lucy H} and Lundie, {Rachel J} and Marley, {Angela K} and Morrison, {Vicky L} and Phythian-Adams, {Alexander T} and Elisabeth Wachter and Webb, {Lauren M} and Sutherland, {Tara E} and Thomas, {Graham D} and Grainger, {John R} and Jim Selfridge and McKenzie, {Andrew N J} and Allen, {Judith E} and Fagerholm, {Susanna C} and Maizels, {Rick M} and Ivens, {Alasdair C} and Adrian Bird and MacDonald, {Andrew S}",
year = "2015",
month = apr,
day = "24",
doi = "10.1038/ncomms7920",
language = "English",
volume = "6",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - A dominant role for the methyl-CpG-binding protein Mbd2 in controlling Th2 induction by dendritic cells

AU - Cook, Peter C

AU - Owen, Heather

AU - Deaton, Aimée M

AU - Borger, Jessica G

AU - Brown, Sheila L

AU - Clouaire, Thomas

AU - Jones, Gareth-Rhys

AU - Jones, Lucy H

AU - Lundie, Rachel J

AU - Marley, Angela K

AU - Morrison, Vicky L

AU - Phythian-Adams, Alexander T

AU - Wachter, Elisabeth

AU - Webb, Lauren M

AU - Sutherland, Tara E

AU - Thomas, Graham D

AU - Grainger, John R

AU - Selfridge, Jim

AU - McKenzie, Andrew N J

AU - Allen, Judith E

AU - Fagerholm, Susanna C

AU - Maizels, Rick M

AU - Ivens, Alasdair C

AU - Bird, Adrian

AU - MacDonald, Andrew S

PY - 2015/4/24

Y1 - 2015/4/24

N2 - 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.

AB - 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.

KW - Allergens

KW - Animals

KW - CD4-Positive T-Lymphocytes

KW - Cell Polarity

KW - Chromatin Immunoprecipitation

KW - DNA Methylation

KW - DNA-Binding Proteins

KW - Dendritic Cells

KW - Enzyme-Linked Immunosorbent Assay

KW - Epigenesis, Genetic

KW - Flow Cytometry

KW - Gene Expression Regulation

KW - Hypersensitivity

KW - Lymphocyte Activation

KW - Mice

KW - Mice, Knockout

KW - Pyroglyphidae

KW - RNA, Messenger

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Schistosoma mansoni

KW - Schistosomiasis mansoni

KW - Th2 Cells

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1038/ncomms7920

DO - 10.1038/ncomms7920

M3 - Journal article

C2 - 25908537

VL - 6

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 6920

ER -