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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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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.

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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.

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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.

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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.

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Intestinal expression of ASBT determines the sclerosing cholangitis phenotype.

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