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

ABSTRACT: Here, we assess chromatin accessibility profiles of naïve CD8+ T cells after 24 hours of exposure to either the LXR agonist RGX-104 or DMSO in the absence of TCR stimulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE303423 | GEO | 2025/12/29

REPOSITORIES: GEO

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

Project description:Here, we analyze transcriptional profiles of naïve CD8+ T cells with versus without exposure to the synthetic LXR agonist RGX-104 in the absence of TCR stimulation.

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

Project description: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.

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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.

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

2025-12-29 | GSE249709 | GEO

scRNA-seq and TCR-seq of T cells and APCs in tumor-draining lymph nodes with versus without pharmacological LXR activation.

Project description:Here we assessed the impact on the transcriptomes of T cells and APCs in tumor-draining lymph nodes from mice administered control chow versus chow containing the synthetic LXR agonist RGX-104. In addition, TCR-seq was performed to assess the impact on clonal expansion of T cells upon LXR activation.

2025-12-31 | GSE275714 | GEO

Immunomodulatory-Photodynamic Nanostimulators for Invoking Pyroptosis to Augment Tumor Immunotherapy

Project description:Acidic tumor microenvironment (TME)-evoked MRC nanoparticles (MRC NPs) co-delivering immune agonist RGX-104 and photosensitizer chlorine e6 (Ce6) are reported for pyroptosis-mediated immunotherapy. RGX-104 remodels TME by transcriptional activation of ApoE to regress myeloid-derived suppressor cells’ (MDSCs) activity, which neatly creates foreshadowing for intensifying pyroptosis. Considering Ce6-triggered photodynamic therapy (PDT) can strengthen oxidative stress and organelles destruction to increase immunogenicity, immunomodulatory-photodynamic MRC nanodrugs will implement an aforementioned two-pronged strategy to enhance gasdermin E (GSDME)-dependent pyroptosis. RNA-seq analysis of MRC at the cellular level is introduced to first elucidate the intimate relationship between RGX-104 acting on LXR/ApoE axis and pyroptosis, where RGX-104 provides the prerequisite for pyroptosis participating in antitumor therapy. Briefly, MRC with favorable biocompatibility tackles the obstacle of hydrophobic drugs delivery, and becomes a powerful pyroptosis inducer to reinforce immune efficacy. MRC-elicited pyroptosis in combination with anti-PD-1 blockade therapy boosts immune response in solid tumors, successfully arresting invasive metastasis and extending survival based on remarkable antitumor immunity. MRC may initiate a new window for immuno-photo pyroptosis stimulators augmenting pyroptosis-based immunotherapy. Owing to the transcriptome sequencing on 4T1 cells exposed to various treatment, pyroptosis mechanism of MRC was thoroughly analyzed via comparing the expression discrepancy among PBS, MRC, and MRC+L groups.

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Bulk RNA-seq of intestinal organoids upon treatment with LXR agonist GW3965

Project description:Liver X Receptor (LXR) activation in intestinal epithelial organoids promotes their growth in vitro. To investigate the downstream effect of LXR activation in intestinal epithelial cells and identify potential pathways driving regeneration, we carried out an unbiased transcriptomic analysis of intestinal epithelial organoids stimulated with the LXR agonist GW3965. In detail, wild type small intestinal crypts were seeded in vitro and stimulated with vehicle (DMSO) or GW3965. After six hours, closing crypts (organoids) were collected for RNA extraction and were analyzed by RNA sequencing.

2023-06-11 | GSE152283 | GEO

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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

Androgen deprivation in PTEN/LXR -/- mice

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2020-07-31 | GSE134137 | GEO

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