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

ABSTRACT: Dendritic cells (DCs) direct CD4+ T cell differentiation into distinct T helper (Th) subsets that are vital for protection against diverse types of infection. However, the mechanisms employed by DCs to initiate Th2 responses, which are important for immunity to helminth infection as well as being a major contributor to allergic disease, remain poorly understood. We demonstrate a crucial role for methyl-CpG-binding domain-2 (Mbd2), a protein that links DNA methylation to repressive chromatin structure, in regulating DC gene expression and ability to promote Th2 immunity against either helminths or allergens.

ORGANISM(S): Mus musculus

PROVIDER: GSE66096 | GEO | 2015/04/20

SECONDARY ACCESSION(S): PRJNA275875

REPOSITORIES: GEO

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

2015-04-20 | E-GEOD-66096 | biostudies-arrayexpress

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

Project description:Dendritic cells (DCs) direct CD4+ T cell differentiation into distinct T helper (Th) subsets that are vital for protection against diverse types of infection. However, the mechanisms employed by DCs to initiate Th2 responses, which are important for immunity to helminth infection as well as being a major contributor to allergic disease, remain poorly understood. We demonstrate a key role for methyl-CpG-binding domain-2 (Mbd2), a protein that 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 displayed reduced phenotypic activation and a dramatically impaired ability to promote Th2 immunity against either helminths or allergens, while their induction of Th1/17 responses remained intact. These data reveal a novel epigenetic mechanism that is integral to DC promotion of CD4+ T cell responses, particularly in Th2 settings, and identify methyl-CpG-binding proteins and the genes that they control as potential therapeutic targets for type-2 inflammation. H3K9,K14ac (H3ac) occupancy was analysed by ChIP-Seq for control (wt) or Mbd2 -/- (DEL) dendritic cells (DC). Input DNA for each cell line was also sequenced alongside.

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Project description:T helper type 2 (Th2) responses are crucial for defense against infections by helminths and are responsible for the development of allergic reactions that can lead to severe clinical disorders, such as asthma or anaphylaxis, and ultimately to death. The induction of Th2 responses requires a specific activation process, triggered by specialized dendritic cells (DCs), by which naive CD4+ Th0 cells acquire the capacity to produce Th2 cytokines. However, the mechanistic basis of the functional specialization enabling DCs for the initiation of Th2 responses has remained elusive. Here we show that interleukin-4 (IL-4), a cytokine produced by basophils, mast cells and Th2-polarized CD4+ T helper cells, exerting a crucial function during anti-helminths and allergic Th2 responses, has a key role in the licensing/conditioning of DCs for the induction of Th2 responses, by bloking their potential to produce Th1-driving cytokines, such as IL-12, IL-18 and IL-23. Microarray analyses (duplicates) were for two types of comparisons: 1. moDCs stimulated with LPS from Escherichia coli versus C-moDCs non stimulated (control). 2. moDCs stimulated with LPS from Escherichia coli in presence of IL4 versus C-moDCs non stimulated (control).

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Role of interleukin-4 in the licensing of dendritic cells for the induction of Th2 responses [B]

Project description:T helper type 2 (Th2) responses are crucial for defense against infections by helminths and are responsible for the development of allergic reactions that can lead to severe clinical disorders, such as asthma or anaphylaxis, and ultimately to death. The induction of Th2 responses requires a specific activation process, triggered by specialized dendritic cells (DCs), by which naive CD4+ Th0 cells acquire the capacity to produce Th2 cytokines. However, the mechanistic basis of the functional specialization enabling DCs for the initiation of Th2 responses has remained elusive. Here we show that interleukin-4 (IL-4), a cytokine produced by basophils, mast cells and Th2-polarized CD4+ T helper cells, exerting a crucial function during anti-helminths and allergic Th2 responses, has a key role in the licensing/conditioning of DCs for the induction of Th2 responses, by bloking their potential to produce Th1-driving cytokines, such as IL-12, IL-18 and IL-23. Microarray analyses (duplicates) were used to compared the transcriptional profile of monocyte-derived dendritic cells (moDCs) cultured with GM-CSF in the absence or presence of interleukin-4: IL4-moDCs versus C-moDCs.

2014-02-19 | E-GEOD-39858 | biostudies-arrayexpress

Role of interleukin-4 in the licensing of dendritic cells for the induction of Th2 responses [B]

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Role of interleukin-4 in the licensing of dendritic cells for the induction of Th2 responses [A]

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Th single cell RNA-Seq

Project description:Th2 cells regulate helminth infections, allergic disorders, tumor immunity and pregnancy by secreting various cytokines. It is likely that there are undiscovered Th2-signaling molecules. While steroids are known to be immunoregulators, de novo steroid production from immune cells has not been previously characterised. We demonstrate production of the steroid pregnenolone by Th2 cells in vitro, and in vivo in a helminth infection model. To identify gene-expression identify of these steroidogenic-Th2 cells, we performed single-cell RNA-sequencing.

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Project description:MARCH1-/- mice have a deficit in TH2 cell development in the mediastinal LN to HDM allergens. Pulmonary DCs that capture allergens and migrate to mediastinal lymph node have been implicated in driving TH2 cell polarization. We then investigated whether MARCH1 is involved in transcriptional reprograming of migratory DCs, which has been suggested to condition the DCs to drive TH2 cell development. To do this, we performed single cell RNA sequencing through the 10X Chromium platform of allergen-carrying WT or MARCH1-/- DCs in the LNs of mice.

2021-09-17 | GSE183861 | GEO

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Project description:The cytokines GM-CSF and IL-5 are thought to possess largely divergent functions despite a shared dependence on the common beta (βC) chain to initiate signaling. Although IL-5 is part of the core type 2 cytokine signature and is required for protection against some helminths, it is dispensable for immunity to others, such as Heligmosomoides polygyrus bakeri (H. polygyrus). Whether this is due to compensatory mechanisms is unclear. The transcription factor Bhlhe40 has been shown to control GM-CSF production and is proposed to be a novel regulator of T helper type 2 cells. We have found that Bhlhe40 is required in T cells for a protective memory response to secondary H. polygyrus infection. H. polygyrus rechallenge elicited dramatic Bhlhe40-dependent changes in gene and cytokine expression by lamina propria CD4+ T cells and in vitro-polarized TH2 cells, including induction of GM-CSF and maximal production of type 2 cytokines including IL-5. βC chain-deficient, but not GM-CSF-deficient, mice rechallenged with H. polygyrus had severely impaired protective immunity. Our results demonstrate that Bhlhe40 is an essential regulator of TH2 cell immunity during helminth infection and reveal unexpected redundancy of βC chain-dependent cytokines.

2019-11-27 | GSE135182 | GEO

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