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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE39858 | GEO | 2014/02/19

SECONDARY ACCESSION(S): PRJNA171887

REPOSITORIES: GEO

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

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).

2014-02-19 | E-GEOD-39862 | biostudies-arrayexpress

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 [A]

2014-02-19 | GSE39862 | GEO

A tissue checkpoint regulates type 2 immunity

Project description:Innate pattern recognition receptors for conserved structural elements play critical roles in immunity against viruses, bacteria and fungi, but analogous pathways linking innate recognition of diverse allergens or helminths with type 2 immunity remain elusive. The discovery of group 2 innate lymphoid cells (ILC2s), which produce similar cytokines as CD4+ T helper 2 (Th2) cells1, has suggested models whereby ILC2s directly or indirectly induce adaptive Th2 cells,2-8 but current understanding of how these cells interact in tissue microenvironments to coordinate allergic immunity is limited. Here, we show that tissue Th2 cells differentiate independently of ILC2s, but that both cell types share overlapping transcriptional and functional programs, which require exposure to the tissue-derived cytokines such as interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP). Combined loss of these epithelial cytokines affects neither Th2 cell priming nor T cell-dependent antibody production, but abrogates allergic lung inflammation due to requirements for local tissue signals to promote differentiation of effector function in both ILC2s and Th2 cells. Our findings reveal how diverse perturbations, including proteases, venoms and mechanical irritants, converge on common pathways to activate type 2 immune responses, thus uncovering a shared checkpoint that can be exploited to control both innate and adaptive allergic inflammation.

2016-10-17 | GSE79703 | GEO

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

2015-04-20 | GSE66096 | GEO

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.

2015-04-20 | E-GEOD-66198 | biostudies-arrayexpress

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

2015-04-20 | GSE66198 | GEO

Single-cell and bulk RNA-seq of Th2

Project description:Th2 cell is a subset of CD4+ T helper (Th) cells, which regulates the immunity to extracellular parasites and allergic inflammation. Th2 cells specifically secrete Type 2 cytokines such as IL-4, IL-5, IL-13, and also express many universal cytokines like IL-2 and GM-CSF. While theses cytokines are indispensable for Th2 cell mediated response, there is complex heterogeneity in the pattern of cytokine production among Th2 cell population. As previous studies were mainly conducted at population levelref, here we took advantage of single-cell RNA-seq to explore heterogeneity in in vitro differentiated Th2 cells. Although a few single cell researches about Th2 cells was conducted, there is no comprehensive understanding of the heterogeneity of Th2 lineage yet, inspiring us to make some difference on this issue. Our studies identify that cytokine genes contributed most to the transcriptome heterogeneity of Th2 cells; expression of universal cytokines showed bimodality, but not Th2 specific cytokines.

2018-11-07 | GSE103647 | GEO

In vivo polarization of Ovalbumin (OVA)-specific CD4 (OTII) T cells

Project description:There remains a need for analysis of CD4 helper T cells differentiation in vivo. To this end ovalbumin (OVA)-specific CD4 (OTII) T cells transferred into congenic mice were studied. Live attenuated OVA-expressing Salmonella (SalOVA) induce T-bet and IFN-g in OTII cells, while alum-precipitated OVA (alumOVA) induces GATA-3 and IL-4. Although 70% of alumOVA-responding OTII cells express GATA-3, only 7% produce IL-4. Thus Th2-polarization defined solely by IL-4 production does not recognize the diversity of GATA-3-expressing effectors. Low-density arrays were designed to assess the expression of 384 genes by real-time RT-PCR. Extensive early diversification occurred in both responses. SalOVA selectively induced many chemokines and pro-inflammatory cytokines, while alumOVA induced few Th2-associated cytokines. Several cytokines and molecules associated with Th17 cells and follicular helper cells were also induced by both antigens. The transcription factor Helios was exclusively induced in alumOVA-responding OTII cells, and critically not in standard in vitro Th2-polarization systems. Early synchronous up-regulation of Helios and GATA-3 mRNA is paralleled at protein level with largely coincident localization in specific nuclear foci of OTII cells responding to alumOVA. This appears to be consistent with a key role for both transcription regulators in the direction of Th2 responses in vivo. Keywords: In vivo T cell polarization Ovalbumin (OVA)-specific CD4 (OTII) T cells were transferred into C57BL/6 mice that were immunized either with live attenuated OVA-expressing Salmonella (Sal) or with alum-precipitated OVA (alum), or not (Naïve). Gene expression assay was performed on FACS sorted OTII cells (Naïve, Sal, Alum). OTII cells were purified from three independent groups of ten naïve, or SalOVA-immunized or alumOVA-immunized mice.

2008-06-27 | E-GEOD-7481 | biostudies-arrayexpress

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