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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE303316 | GEO | 2025/12/30

REPOSITORIES: GEO

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

Project description: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.

2025-12-29 | GSE303423 | GEO

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.

2025-12-29 | GSE249707 | GEO

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.

2025-12-30 | GSE249710 | GEO

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

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

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

| PRJNA1295387 | ENA

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.

2023-08-13 | GSE240328 | GEO

RNA Sequencing in LXR agonist fed Atp7b-/- mice (Wilson disease)

Project description:The goal of the study was find the gene expression of diverse signaling pathways altered in Atp7b-/- mice (murine WD) liver as compared to control mice and how LXR agonist treatment will improve/ameliorate WD phenotype in Atp7b-/- mice. Activation of LXR/RXR using synthetic LXR agonist ameliorates liver inflammation and fibrosis in murine WD by changing gene expression.

2022-10-26 | GSE174015 | GEO

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

Genome-wide profiling of LXR, RXR and PPARM-NM-1 in mouse liver reveals extensive sharing of binding sites

Project description:The liver X receptors (LXRs) are nuclear receptors that form permissive heterodimers with retinoid X receptor (RXR) and are important regulators of lipid metabolism in the liver. We have recently shown that RXR agonist-induced hypertriglyceridemia and hepatic steatosis in mice is dependent on LXR and correlates with an LXR-dependent hepatic induction of lipogenic genes. To further investigate the role of RXR and LXR in the regulation of hepatic gene expression, we have mapped the ligand-regulated genome-wide binding of these factors in mouse liver. We find that the RXR agonist bexarotene primarily increases the genomic binding of RXR, whereas the LXR agonist T0901317 greatly increases both LXR and RXR binding. Functional annotation of putative direct LXR target genes revealed a significant association with classical LXR-regulated pathways as well as PPAR signaling pathways, and subsequent ChIP-seq mapping of PPARM-NM-1 binding demonstrated binding of PPARM-NM-1 to 71-88% of the identified LXR:RXR binding sites. Sequence analysis of shared binding regions combined with sequential ChIP on selected sites indicate that LXR:RXR and PPARM-NM-1:RXR bind to degenerate response elements in a mutually exclusive manner. Together our findings suggest extensive and unexpected cross-talk between hepatic LXR and PPARM-NM-1 at the level of binding to shared genomic sites LXR, RXR, PPARalpha and RNA Polymerase II ChIP-seq on livers from female C57BL/6 wild-type and/or LXRM-NM-1/M-NM-2-deficient mice (13 weeks of age, n=1) treated by oral gavage once daily for 14 days with the RXR agonist bexarotene (100 mg/kg body weight [mpk], in 1% carboxymethylcellulose), the LXR agonist T0901317 (T09, 30 mpk) or vehicle alone.

2012-01-31 | E-GEOD-35262 | biostudies-arrayexpress

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