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The intestine harbours functionally distinct tissue-resident and inflammatory Th17 cells

ABSTRACT: The intestine harbours functionally distinct tissue-resident and inflammatory Th17 cells

PROVIDER: PRJNA535435 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8955160_1.fastq.gz	Fastqsanger.gz
	SRR8955160_2.fastq.gz	Fastqsanger.gz
	SRR8955161_1.fastq.gz	Fastqsanger.gz
	SRR8955161_2.fastq.gz	Fastqsanger.gz
	SRR8955152_1.fastq.gz	Fastqsanger.gz

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The intestine harbours functionally distinct tissue-resident and inflammatory Th17 cells

Project description:Th17 cells are extensively studied because of their known pathogenic role in many inflammatory diseases, but are also important to support the integrity of the intestinal barrier in a non-inflammatory manner. Since therapeutic targeting of Th17 cell mediated pathologies carries the risk of inadvertently affecting protective Th17 cells, we set out to define the major distinctions between homeostatic tissue-resident Th17 cells and Th17 cells engaged in inflammatory reactions, focusing on the gut. We show here that homeostatic Th17 cells exhibit little plasticity towards expression of inflammatory cytokines, are characterised by a metabolism typical for quiescent or memory T cells, and do not participate in inflammatory processes. Infection-induced Th17 cells, on the other hand, show extensive plasticity towards pro-inflammatory cytokines, disseminate widely into the periphery and engage aerobic glycolysis in addition to oxidative phosphorylation typical for inflammatory effector cells.

2019-06-28 | GSE130302 | GEO

The Intestine Harbors Functionally Distinct Homeostatic Tissue-Resident and Inflammatory Th17 Cells.

Project description:T helper 17 (Th17) cells are pathogenic in many inflammatory diseases, but also support the integrity of the intestinal barrier in a non-inflammatory manner. It is unclear what distinguishes inflammatory Th17 cells elicited by pathogens and tissue-resident homeostatic Th17 cells elicited by commensals. Here, we compared the characteristics of Th17 cells differentiating in response to commensal bacteria (SFB) to those differentiating in response to a pathogen (Citrobacter rodentium). Homeostatic Th17 cells exhibited little plasticity towards expression of inflammatory cytokines, were characterized by a metabolism typical of quiescent or memory T cells, and did not participate in inflammatory processes. In contrast, infection-induced Th17 cells showed extensive plasticity towards pro-inflammatory cytokines, disseminated widely into the periphery, and engaged aerobic glycolysis in addition to oxidative phosphorylation typical for inflammatory effector cells. These findings will help ensure that future therapies directed against inflammatory Th17 cells do not inadvertently damage the resident gut population.

| S-EPMC6642154 | biostudies-literature

Inflammatory Th1 and Th17 in the Intestine Are Each Driven by Functionally Specialized Dendritic Cells with Distinct Requirements for MyD88.

Project description:Normal dynamics between microbiota and dendritic cells (DCs) support modest numbers of T cells, yet these do not cause inflammation. The DCs that induce inflammatory T cells and the signals that drive this process remain unclear. Here, we demonstrate that small intestine DCs lacking the signaling attenuator A20 induce inflammatory T cells and that the signals perceived and antigen-presenting cell (APC) functions are unique for different DC subsets. Thus, although CD103+CD11b- DCs exclusively instruct IFN?+ T cells, CD103+CD11b+ DCs exclusively instruct IL-17+ T cells. Surprisingly, APC functions of both DC subsets are upregulated in a MyD88-independent fashion. In contrast, CD103-CD11b+ DCs instruct both IFN?+ and IL-17+ T cells, and only the IL-17-inducing APC functions require MyD88. In disease pathogenesis, both CD103-CD11b+ and CD103+CD11b+ DCs expand pathologic Th17 cells. Thus, in disease pathogenesis, specific DCs instruct specific inflammatory T cells.

| S-EPMC5123685 | biostudies-literature

Divergent molecular networks program functionally distinct CD8+ skin-resident memory T cells

Project description:Divergent molecular networks program functionally distinct CD8+ skin-resident memory T cells

| PRJNA976184 | ENA

Human intestinal tissue-resident memory T cells comprise transcriptionally and functionally distinct subsets

Project description:Human intestinal tissue-resident memory T cells comprise transcriptionally and functionally distinct subsets

| PRJNA682612 | ENA

Selective induction of homeostatic Th17 cells in the murine intestine by cholera toxin interacting with the microbiota

Project description:Th17 cells play a role as an inflammation mediator in a variety of autoimmune disorders, including inflammatory bowel disease (IBD) and thus are widely considered to be pathogenic. However, Th17 cells are present in the normal intestine and show a homeostatic phenotype, i.e., they participate in the maintenance of intestinal homeostasis rather than inducing inflammation. We observed an enlarged Th17 population in the small intestine of C57BL/6.IgA-/- mice compared to wild-type mice, which was further amplified with cholera toxin (CT) immunization without causing intestinal inflammation. The increased Th17 induction and the correspondingly 10-fold higher CTB-specific serum IgG response in C57BL/6.IgA-/- mice after CT immunization was microbiota dependent and was associated with increased segmented filamentous bacteria (SFB) in the small intestine of C57BL/6.IgA-/- mice. Oral administration of vancomycin greatly dampened both CT immunogenicity and adjuvanticity, and the differential CT responses in IgA-/- and wild-type mice disappeared after intestinal microbiota equalization. Using gnotobiotic mouse models, we found that CT induction of homeostatic intestinal Th17 responses was supported not only by SFB but also by other commensal bacteria. Furthermore, transcriptome analysis using IL-17AhCD2 reporter mice revealed a similar gene expression profile in CT-induced intestinal Th17 cells and endogenous intestinal Th17 cells at homeostasis, with upregulated expressions of a panel of immune regulatory genes, which was distinctly different from the gene expression profile of pathogenic Th17 cells. Taken together, we identified a non-pathogenic signature of intestinal homeostatic Th17 cells, which are actively regulated by the commensal microbiota and can be selectively stimulated by CT.

2017-08-31 | GSE97571 | GEO

Human intestinal tissue-resident memory T cells comprise transcriptionally and functionally distinct subsets II

Project description:Human intestinal tissue-resident memory T cells comprise transcriptionally and functionally distinct subsets II

| PRJNA682615 | ENA

Human intestinal tissue-resident memory T cells comprise transcriptionally and functionally distinct subsets I

Project description:Human intestinal tissue-resident memory T cells comprise transcriptionally and functionally distinct subsets I

| PRJNA682613 | ENA

Epithelial miR-215 negatively modulates Th17-dominant inflammation by inhibiting CXCL12 production in the small intestine

Project description:MicroRNAs are a class of non-coding short-chained RNAs that control cellular functions by downregulating their target genes. Recent research indicates that microRNAs play a role in the maintenance of gut homeostasis. miR-215 was found to be highly expressed in epithelial cells of the small intestine; however, the involvement of miR-215 in gut immunity remains unknown. Here, we show that miR-215 negatively regulates inflammation in the small intestine by inhibiting CXCL12 production. Mice lacking miR-215 showed high susceptibility to inflammation induced by indomethacin, accompanied by an increased number of Th17 cells in the lamina propria of the small intestine. Our findings support a promising perspective of targeting miR-215 to treat inflammatory conditions in the small intestine.

2022-01-27 | GSE186708 | GEO

Resident memory CD8 T cells persist for years in human small intestine

Project description:Resident memory CD8 T cells (Trm) have been shown to provide effective protective responses in the small intestine (SI) in mice. A better understanding of the generation and persistence of SI CD8 Trm cells in humans may have implications for intestinal immune-mediated diseases and vaccine development. Analyzing normal and transplanted human SI we demonstrated that the majority of SI CD8 T cells were bona fide CD8 Trm cells that survived for over 1 year in the graft. Intraepithelial and lamina propria CD8 Trm cells showed a high clonal overlap and a repertoire dominated by expanded clones, conserved both spatially in the intestine and over time. Functionally, lamina propria CD8 Trm cells were potent cytokine-producers, exhibiting a polyfunctional (IFN-γ+ IL-2+ TNF-α+) profile, and efficiently expressed cytotoxic mediators after stimulation. These results suggest that SI CD8 Trm cells could be relevant targets for future oral vaccines and therapeutic strategies for gut disorders.

| EGAS00001003676 | EGA

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