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Single-cell Atlas of intrahepatic T cells reveals a population of liver-resident naive-like CD4+ T cells expanded in primary sclerosing cholangitis

ABSTRACT: Single-cell Atlas of intrahepatic T cells reveals a population of liver-resident naive-like CD4+ T cells expanded in primary sclerosing cholangitis

PROVIDER: PRJEB52042 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	ERR9467480_1.fastq.gz	Fastqsanger.gz
	ERR9467480_2.fastq.gz	Fastqsanger.gz
	ERR9467490_1.fastq.gz	Fastqsanger.gz
	ERR9467490_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Single-cell Atlas of intrahepatic T cells reveals a population of liver-resident naive-like CD4+ T cells expanded in primary sclerosing cholangitis

Project description:The composition of intrahepatic immune cells in primary sclerosing cholangitis (PSC) and their contribution to disease pathogenesis is widely unknown. We here generated a single-cell atlas of intrahepatic T cells in PSC, a type of immune cells that has previously been involved in the pathogenesis of PSC. This atlas provides a valuable data source to the field. Using that atlas, we identified a population of liver-resident naive-like CD4+ T cells which are expanded in livers of patients with PSC compared to healthy and other liver diseases. Trajectory inference suggest that these cells have a propensity to acquire TH17-associated effector functions. Using blood-derived cells naive CD4+ T cells we experimentally prove this propensity. Since TH17-polarized cells are considered to contribute to the development of PSC, our findings point towards a so far underestimated role of naive T cells in PSC.

2021-03-27 | E-MTAB-10143 | biostudies-arrayexpress

Inflammatory type 2 conventional dendritic cells contribute to murine and human cholangitis

Project description:Cholangitis mouse models were characterised by selective intrahepatic expansion of type 2 conventional dendritic cells, whereas plasmacytoid and type 1 conventional dendritic cells were not expanded. Expansion of type 2 conventional dendritic cells in human PSC lesions was confirmed by histology. Depletion studies revealed a pro-inflammatory role of type 2 conventional dendritic cells. Single-cell transcriptomics confirmed inflammatory maturation of the intrahepatic type 2 conventional dendritic cells and identified dendritic cell-derived inflammatory mediators.

2022-07-08 | E-MTAB-11821 | biostudies-arrayexpress

STAT3 protects from liver injury and fibrosis in a mouse model of sclerosing cholangitis

Project description:Background and aims: Signal transducer and activator of transcription 3 (Stat3) is the main mediator of interleukin-6 type cytokine signaling required for hepatocyte proliferation and hepatoprotection but its role in sclerosing cholangitis and other cholestatic liver diseases remains unresolved. Methods: We investigated the role of Stat3 in inflammation-induced cholestatic liver injury and used mice lacking the multidrug resistance gene 2 (mdr2-/-) as a model for SC. Results: We demonstrate that conditional inactivation of stat3 in hepatocytes and cholangiocytes (stat3 delta hc) of mdr2-/- mice strongly aggravated bile acid-induced liver injury and fibrosis. A similar phenotype was observed in mdr2-/- mice lacking IL-6 production. Biochemical and molecular characterization suggested that Stat3 exerts hepatoprotective functions in both, hepatocytes and cholangiocytes. Loss of Stat3 in cholangiocytes led to increased expression of TNFÎ± which might reduce the barrier function of bile ducts. Loss of Stat3 in hepatocytes led to upregulation of bile acid biosynthesis genes and downregulation of hepatoprotective epidermal growth factor receptor and insulin-like growth factor 1 signaling pathways. Consistently, stat3deltahc mice were more sensitive to cholic acid-induced liver damage than control mice. Conclusions: Our data suggest that Stat3 prevents cholestasis and liver damage in sclerosing cholangitis via regulation of pivotal functions in hepatocytes and cholangiocytes. Affymetrix microarray analyses was performed to identify metabolic and molecular pathways in stat3Dhc mdr2-/- mice that lead to cholestasis and bile acid-induced liver injury. To avoid false positive results that are due to differential cellular composition, we defined the onset of fibrosis and expression of fibrogenic factors in stat3Dhc mdr2-/- mice.

2010-10-20 | E-GEOD-18759 | biostudies-arrayexpress

Downregulation of TGR5 (GPBAR1) in biliary epithelial cells is characteristic of sclerosing cholangitis and may contribute to disease pathogenesis

Project description:Primary sclerosing cholangitis (PSC) is characterized by chronic inflammation and progressive fibrosis of the biliary tree. The bile acid receptor TGR5 is found on biliary epithelial cells (BECs), where it promotes secretion, proliferation and tight junction integrity. Thus, we speculated that changes in TGR5 expression in BECs may contribute to PSC pathogenesis.

2021-03-12 | GSE168758 | GEO

Intestinal expression of ASBT determines the sclerosing cholangitis phenotype.

Project description:Intestinal expression of ASBT determines the sclerosing cholangitis phenotype.

| PRJNA546456 | ENA

Gene expression profiles of sclerosing cholangitis activity in mice

Project description:Background. Abcb4 (-/-) mice secrete phosphatidylcholine-deficient bile and develop sclerosing cholangitis (SC). The cholangitis involves differential hepatic transcription of genes whose products govern inflammation, activation of hepatic stellate cells and fibrosis. This study was undertaken to test the hypothesis that several genes involved in regulation of tissue inflammation and fibrosis display transcription rates that reflect SC disease activity. Methods. Abcb4 (-/-) mice fed cholic acid (CA) display high SC activity and ursodeoxycholic acid (UDCA) fed mice display low SC activity. Differential hepatic transcription of genes was accordingly measured in abcb4 (-/-) mice maintained on CA- and UDCA-supplemented diets using cDNA microarrays. Abcb4 (+/+) mice served as controls. The differential transcription of selected genes was verified by real time polymerase chain reaction. Liver tissue pathology was quantified by histopathology scoring and immunohistochemistry to visualize bile duct cells and activated hepatic stellate cells. Results. Differential transcription of Ccl2, Ccl20, Cxcl10, Nfκb1, Nfκb2, Tgfβ1, Tgfβ2, Sparc, Ctgf, Lgals3, Elf3, Spp1, Pdgfa, Pdgfrb, Col1a1, Col1a2 and Col4a1 genes paralleled the differing SC activities of cholic acid- and UDCA-fed abcb4 (-/-) mice. Histopathology scores and immunohistochemistry showed greatly enhanced activation of hepatic stellate cells during high SC activity due to CA feeding. Conclusion. Differential transcription of several genes relating to tissue inflammation and hepatic stellate cell activation parallels SC activity in abcb4 (-/-) mice. Data on their differential transcription may be used to gauge SC disease activity.

2008-08-20 | GSE11507 | GEO

Il-17 Signaling in Primary Sclerosing Cholangitis Patient-Derived Organoids

Project description:Il-17 Signaling in Primary Sclerosing Cholangitis Patient-Derived Organoids

| PRJNA998754 | ENA

CCL24 regulates biliary inflammation and fibrosis in primary sclerosing cholangitis

Project description:CCL24 regulates biliary inflammation and fibrosis in primary sclerosing cholangitis

| PRJNA950414 | ENA

Bile Acid of Primary Sclerosing Cholangitis (part IV)

Project description:To qualitatively and quantitatively analyze enterohepatically-circulated molecules using targeted bile acid concentrations of peripheral blood collected from primary sclerosing cholangitis (PSC) patients compared to normal and diseased controls. There are three groups of patients. (1) Normal donor controls (ND), (2) Patients with Primary Sclerosing Cholangitis (PSC), and (3) Disease Controls (DC) which are patients with liver disease other than PSC.

2017-07-05 | ST000998 | MetabolomicsWorkbench

CCL24 regulates biliary inflammation and fibrosis in primary sclerosing cholangitis

Project description:CCL24 is a profibrotic, proinflammatory chemokine expressed in several chronic fibrotic diseases. In the liver, CCL24 plays a role in fibrosis and inflammation and blocking CCL24 led to reduced liver injury in experimental models. We studied the role of CCL24 in primary sclerosing cholangitis (PSC) and evaluated the potential therapeutic effect of blocking CCL24 in this disease. Mdr2-/- mice demonstrated CCL24 expression in liver macrophages and were used as a relevant experimental PSC model. CCL24 neutralizing monoclonal antibody, CM-101, significantly improved inflammation, fibrosis and cholestasis-related markers in the biliary area. Moreover, using spatial transcriptomics we observed reduced proliferation and senescence of cholangiocytes following CCL24 neutralization. Next, we demonstrated that CCL24 expression was elevated under profibrotic conditions in primary human cholangiocytes and macrophages and it induced proliferation of primary human hepatic stellate cells and cholangiocytes, which was attenuated following CCL24 inhibition. Correspondingly, CCL24 was found to be highly expressed in liver biopsies of PSC patients. CCL24 serum levels correlated with Enhanced Liver Fibrosis score, most notably in patients with high alkaline phosphatase levels. These results suggest that blocking CCL24 may have a therapeutic effect in PSC patients via reduced liver inflammation, fibrosis and cholestasis.

2023-04-30 | GSE228596 | GEO

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