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Epidermal growth factor receptor expression licenses T helper-2 cells to function in a T cell receptor-independent fashion

ABSTRACT: Epidermal growth factor receptor expression licenses T helper-2 cells to function in a T cell receptor-independent fashion

PROVIDER: PRJNA408233 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6056720.fastq.gz	Fastqsanger.gz
	SRR6058060.fastq.gz	Fastqsanger.gz
	SRR6056721.fastq.gz	Fastqsanger.gz
	SRR6058051.fastq.gz	Fastqsanger.gz
	SRR6058061.fastq.gz	Fastqsanger.gz

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Epidermal growth factor receptor expression licenses T helper-2 cells to function in a T cell receptor-independent fashion

Project description:Gastro-intestinal helminth infections trigger the release of interleukin-33 (IL-33), which induces type 2 helper T-cells (Th2 cells) at the site of infection to produce IL-13, thereby contributing to host resistance in a T cell receptor (TCR)-independent manner. Here we show that as a prerequisite for IL-33 induced IL-13 secretion, Th2 cells required the expression of the Epidermal Growth Factor Receptor (EGFR) and of its ligand, Amphiregulin, for the formation of a signaling complex between T1/ST2 (the IL-33R) and EGFR. This shared signaling complex allowed IL-33 to induce the EGFR-mediated activation of the MAP-kinase signaling pathway and consequently the expression of IL-13. Lack of EGFR expression on T cells abrogated IL-13 expression in infected tissues and impaired host resistance. EGFR expression on Th2 cells was TCR-signaling dependent, and therefore our data reveal a mechanism by which antigen-presentation controls the innate effector function of Th2 cells at the site of inflammation.

2017-09-22 | GSE104096 | GEO

Epidermal Growth Factor Receptor Expression Licenses Type-2 Helper T Cells to Function in a T Cell Receptor-Independent Fashion.

Project description:Gastro-intestinal helminth infections trigger the release of interleukin-33 (IL-33), which induces type-2 helper T cells (Th2 cells) at the site of infection to produce IL-13, thereby contributing to host resistance in a T cell receptor (TCR)-independent manner. Here, we show that, as a prerequisite for IL-33-induced IL-13 secretion, Th2 cells required the expression of the epidermal growth factor receptor (EGFR) and of its ligand, amphiregulin, for the formation of a signaling complex between T1/ST2 (the IL-33R) and EGFR. This shared signaling complex allowed IL-33 to induce the EGFR-mediated activation of the MAP-kinase signaling pathway and consequently the expression of IL-13. Lack of EGFR expression on T cells abrogated IL-13 expression in infected tissues and impaired host resistance. EGFR expression on Th2 cells was TCR-signaling dependent, and therefore, our data reveal a mechanism by which antigen presentation controls the innate effector function of Th2 cells at the site of inflammation.

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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis.

Project description:MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis.

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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis

Project description:MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis

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The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

Project description:The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

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OPTImal PALliative Anti-epidermal Growth Factor Receptor Treatment in Metastatic Colorectal Cancer -

Project description:The present study will investigate the feasibility and clinical value of using circulating tumor DNA as selection for anti-epidermal growth factor receptor treatment for metastatic colorectal cancer.

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The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

Project description:The M3 muscarinic acetylcholine receptor (CHRM3) is predominantly expressed in the basal epidermal layer where it mediates the effects of the auto/paracrine cytotransmitter acetylcholine. Patients with the autoimmune blistering disease pemphigus develop autoantibodies to CHRM3 and show alterations in keratinocyte adhesion, proliferation and differentiation, suggesting that CHRM3 controls these cellular functions. Chrm3 mice display altered epidermal morphology resembling that seen in patients with pemphigus vulgaris. Here, we characterized the cellular and molecular mechanisms whereby CHRM3 controls epidermal structure and function. We used single cell (sc)RNA-seq to evaluate keratinocyte heterogeneity and identify differentially expressed genes in specific subpopulations of epidermal cells in Chrm3 KO neonatal mice.

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Two unequally redundant 'helper' immune receptor families mediate Arabidopsis intracellular 'sensor' immune receptor functions

Project description:Two unequally redundant 'helper' immune receptor families mediate Arabidopsis intracellular 'sensor' immune receptor functions

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