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A human TH17 population with a tissue-resident signature in healthy and inflamed oral mucosal tissues [Bulk RNA-seq]

ABSTRACT: A human TH17 population with a tissue-resident signature in healthy and inflamed oral mucosal tissues [Bulk RNA-seq]

PROVIDER: PRJNA477371 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7410100.fastq.gz	Fastqsanger.gz
	SRR7410110.fastq.gz	Fastqsanger.gz
	SRR7410120.fastq.gz	Fastqsanger.gz
	SRR7410101.fastq.gz	Fastqsanger.gz
	SRR7410111.fastq.gz	Fastqsanger.gz

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A human TH17 population with a tissue-resident signature in healthy and inflamed oral mucosal tissues [10x]

Project description:T cells in mucosal tissues fulfill a complex array of duties to ensure maintenance of barrier immunity. In oral mucosa tissue, we found that increased inflammation altered CD4 T cell subsets in a spatially-dependent manner, although it had a modest effect on the frequency of tissue-resident memory T cells (TRM) and the CD4 T cell transcriptome. In contrast, localization to the tissue profoundly altered the transcriptional profile, emphasizing the importance of studying healthy tissue to understand disease-specific changes. Our data revealed the existence of a TH17 cell population that is predominantly found in the tissue-resident, but not transient, CD4 T cell compartment in mucosal tissue.

2019-12-08 | GSE116130 | GEO

A human TH17 population with a tissue-resident signature in healthy and inflamed oral mucosal tissues [Bulk RNA-seq]

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A human TH17 population with a tissue-resident signature in healthy and inflamed oral mucosal tissues

Project description:A human TH17 population with a tissue-resident signature in healthy and inflamed oral mucosal tissues

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A human TH17 population with a tissue-resident signature in healthy and inflamed oral mucosal tissues [10x]

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A human TH17 population with a tissue-resident signature in healthy and inflamed oral mucosal tissues

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:The single-cell transcriptomes were performed from paired uninflamed and inflamed mucosal biopsies obtained from surgically resected colonic samples from 3 CD patients.

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Dysbiotic microbiome triggers Th17 cells to mediate oral mucosal immunopathology in mice and humans

Project description:Animal model implicates microbiota-triggered oral mucosal Th17 cells as drivers of local immunopathology and therapeutic targets in periodontitis.

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Mouse Th17 T cells, IL-23 stimulated

Project description:Interleukin 23 (IL-23) triggers pathogenic features in pro-inflammatory, IL-17-secreting T cells (Th17 and Tγδ17) that play a key role in the development of inflammatory diseases. However, the IL-23 signaling cascade remains largely undefined. Here we used quantitative phosphoproteomics to characterize IL-23 signaling in primary murine Th17 cells. We quantified 6,888 phosphorylation sites in Th17 cells, and found 168 phosphorylations regulated upom IL-23 stimulation. IL-23 increased the phosphorylation of the myosin regulatory light chain (RLC), an actomyosin contractibility marker, in Th17 and Tγδ cells. IL-23-induced RLC phosphorylation required JAK2 and ROCK catalytic activity, and the study of the IL-23/ROCK axis revealed an unexpected role of IL-23 in the migration of Tγδ17 and Th17 cells. Moreover, pharmacological inhibition of ROCK reduced Tγδ17 recruitment to inflamed skin upon challenge with inflammatory agent Imiquimod. This work: i) provides new insights into phosphorylation networks that control Th17 cells, ii) widely expands the current knowledge on IL-23 signaling, and iii) contributes to the increasing list of immune cells subsets characterized by global phosphoproteomic approaches.

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Th17 pathway is activated in early inflamed acne lesions

Project description:The mechanisms of inflammation in acne are not well understood. This study performed in two separate patient populations focused on the activation of adaptive and innate immunity in early inflamed acne. Biopsies were collected from lesional and non-lesional skin of acne patients. Psoriasis patients and healthy volunteers were included in the study for comparison (not included in the records). Using Affymetrix Genechips, we observed significant elevation of the signature cytokines of the Th17 lineage in acne lesions compared to non-lesional skin. The increased expression of IL-17 was confirmed with real-time qPCR (RT-PCR) in two separate patient populations. Cytokines involved in Th17 lineage differentiation (IL-1beta, IL-6, TGF-beta; IL23p19) were remarkably induced at the RNA level. In addition, pro-inflammatory cytokines (IL-8, TNF-α), Th1 markers (IL12p40, CXCR3, T-bet, IFN-gamma), T regulatory cell markers (Foxp3, IL-10, TGF-β) and antimicrobial peptides (S100A7, S100A9, LNC2, hBD2, hBD3, hCAP18) were induced. Importantly, immunohistochemistry revealed significantly increased numbers of IL-17A positive T cells and CD83 dendritic cells in the acne lesions. In summary our results demonstrate the presence of IL17A positive T cells and the activation of Th17-related cytokines in acne lesions, indicating that the Th17 pathway may play a pivotal role in the disease process, offering new targets of therapy.

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