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Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis I

ABSTRACT: We study the effect of Treg cell-derived Areg in chronic liver injury. Here we look at the transcriptional changes of Treg cells in fibrosis compared to control and conventional T cells in vivo.

ORGANISM(S): Mus musculus

PROVIDER: GSE208641 | GEO | 2024/02/02

REPOSITORIES: GEO

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Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis [scHSC]

Project description:We study the effect of Treg cell-derived Areg in chronic liver injury. Here we look at the transcriptional changes of hepatic stellate cells in NASH in response to Treg cell-derived Areg.

2024-02-02 | GSE234073 | GEO

Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis II

Project description:We study the effect of Treg cell-derived Areg on hepatic stellate cells. Here we look at the transcriptional effect of Areg on hepatic stellate cells in vitro.

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Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis [scTreg]

Project description:We study the effect of Treg cell-derived Areg in chronic liver injury. Here we look at the transcriptional changes of Treg cells in NASH compared to normal chow.

2024-02-02 | GSE234244 | GEO

Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis.

Project description:Production of amphiregulin (Areg) by regulatory T (Treg) cells promotes repair after acute tissue injury. Here, we examined the function of Treg cells in non-alcoholic steatohepatitis (NASH), a setting of chronic liver injury. Areg-producing Treg cells were enriched in the livers of mice and humans with NASH. Deletion of Areg in Treg cells, but not in myeloid cells, reduced NASH-induced liver fibrosis. Chronic liver damage induced transcriptional changes associated with Treg cell activation. Mechanistically, Treg cell-derived Areg activated pro-fibrotic transcriptional programs in hepatic stellate cells via epidermal growth factor receptor (EGFR) signaling. Deletion of Areg in Treg cells protected mice from NASH-dependent glucose intolerance, which also was dependent on EGFR signaling on hepatic stellate cells. Areg from Treg cells promoted hepatocyte gluconeogenesis through hepatocyte detection of hepatic stellate cell-derived interleukin-6. Our findings reveal a maladaptive role for Treg cell-mediated tissue repair functions in chronic liver disease and link liver damage to NASH-dependent glucose intolerance.

| S-EPMC10922825 | biostudies-literature

Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis

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

2024-02-02 | GSE208706 | GEO

An amphiregulin reporter mouse enables transcriptional and clonal expansion analysis of reparative lung Treg cells

Project description:Treg cells play critical roles in tissue repair processes, certain of which are mediated by production of the growth factor amphiregulin (Areg). We developed a knock-in mouse model for detection of Areg production in live Treg cells, inserting a Thy1a (Thy1.1) construct into the endogenous Areg locus, such that for every transcript of Areg that is translated, a Thy1.1 transcript is also translated and trafficked separately to the cell surface. We used this mouse model to sort for Thy1.1- or Thy1.1+ (Areg-producing or -non-producing) lung Treg cells in models of lung damage (influenza A virus infection and bleomycin acute lung injury), and used them for assessment of gene expression and clonal expansion of these populations.

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