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LXR agonism promotes T cell effector chromatin landscapes upon crosspriming by dendritic cells.

ABSTRACT: Here, we assess chromatin accessibility profiles of OT-I CD8+ T cells upon co-culture with antigen-pulsed BMDCs in the presence or absence of the synthetic LXR agonist RGX-104.

ORGANISM(S): Mus musculus

PROVIDER: GSE249707 | GEO | 2025/12/29

REPOSITORIES: GEO

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LXR agonism enhances T cell activation upon crosspresentation by LXR-DKO BMDCs.

Project description:Here, we analyze transcriptional profiles of OT-I CD8+ T cells co-cultured with LXR-/- bone marrow-derived dendritic cells pulsed with the SIINFEKL peptide in the absence or presence of the synthetic LXR agonist RGX-104.

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LXR agonism enhances T cell activation upon crosspresentation.

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LXR agonism elicits a pre-effector state in naïve CD8+ T cells [RNA-seq]

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LXR agonism elicits a pre-effector state in naïve CD8+ T cells [ATAC-seq]

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Immunomodulatory-Photodynamic Nanostimulators for Invoking Pyroptosis to Augment Tumor Immunotherapy

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2024-01-26 | PXD039035 | Pride

In vivo screen identifies LXR agonism potentiates sorafenib killing of hepatocellular carcinoma

Project description:Background & Aims: Existing drug therapies for hepatocellular carcinoma (HCC), including sorafenib, extend patient survival by only three months. We sought to identify novel druggable targets for use in combination with sorafenib to increase its efficacy. Methods: We implemented an in vivo genetic screening paradigm utilizing a library of 43 genes-of-interest expressed in the context of repopulation of the injured livers of Fumarylacetoacetate Hydrolase-deficient (Fah-/-) mice, which led to highly penetrant HCC. We treated mice with vehicle or sorafenib, then determined the genetic drivers of each tumor from the library. Liver X Receptor alpha (LXRalpha) emerged as a potential target. To examine LXRalpha agonism in combination with sorafenib treatment, we added varying concentrations of sorafenib and LXRalpha agonist drugs to HCC cell lines. To elucidate the mechanism of tumor death, we performed transcriptomic analysis. Results: Fah-/- mice injected with the screening library developed HCC tumor clones containing Myc cDNA plus various other cDNAs. Treatment with sorafenib resulted in sorafenib-resistant HCCs that were significantly depleted in Nr1h3 cDNA, encoding LXRalpha, suggesting that LXRalpha activation is incompatible with tumor growth in the presence of sorafenib treatment in vivo. Combination treatment using sorafenib and LXR agonist drugs in multiple HCC cell lines led to enhanced cell death as compared to monotherapy, due to reduced expression of cell cycle regulators and increased expression of genes associated with apoptosis. Combination therapy also enhanced cell death in a sorafenib-resistant primary human HCC cell line. Conclusions: We have completed a novel drug resistance screen in vivo, and identified that LXR agonism potentiates the efficacy of sorafenib in treating HCC.

2020-05-29 | GSE151412 | GEO

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