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Gene expression profile of Cd45 positive cells in single cell level from KRASLSL.G12D/+P53LSL.R172H/+Pdx-Cre mice (KPC tumor mouse) model treated with stimulator of interferon genes (STING) and lymphotoxin-beta receptor (LTbR) agonist [2024_v2]

ABSTRACT: Gene expression profile of Cd45 positive cells in single cell level from KRASLSL.G12D/+P53LSL.R172H/+Pdx-Cre mice (KPC tumor mouse) model treated with stimulator of interferon genes (STING) and lymphotoxin-beta receptor (LTbR) agonist [2024_v2]

PROVIDER: PRJNA1153447 | ENA |

REPOSITORIES: ENA

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Gene expression profile of Cd45 positive cells in single cell level from KRASLSL.G12D/+P53LSL.R172H/+Pdx-Cre mice (KPC tumor mouse) model treated with stimulator of interferon genes (STING) and lymphotoxin-beta receptor (LTbR) agonist

Project description:The combination treatment using STING and LTbR agonists improves the immune landscape in KPC tumor model. We used single-cell RNA sequence (scRNAseq) analysis to investigate the characteristics of Cd45 positive cells after treating the tumor.

2025-07-22 | GSE275840 | GEO

2025-07-22 | GSE275876 | GEO

Project description:Gene expression profile of Cd45 positive cells in single cell level from KRASLSL.G12D/+P53LSL.R172H/+Pdx-Cre mice (KPC tumor mouse) model treated with stimulator of interferon genes (STING) and lymphotoxin-beta receptor (LTbR) agonist

| PRJNA1153279 | ENA

Comprehensive understanding the molecular components of LTBR signalling complex in cancers

Project description:Lymphotoxin beta receptor (LTBR), a member of TNFRSF, was identified as a key regulator in the development, organization, and homeostasis of lymphoid tissues (Wolf, Seleznik, Zeller, & Heikenwalder, 2010). Recently, LTBR has been shown to play a role in tumor biology, both in solid tumors and in hematological cancers (Fernandes et al., 2016; Haybaeck et al., 2009; Lo et al., 2007). However, the role of LTBR in cancer biology is still controversial. From the perspective of tumor eradication, the combination of LIGHT and IFN-g can induce apoptotic cell death in HT29 cells and some other cell lines via the increase of intracellular reactive oxygen species (ROS) (Chang, Chao, Hsieh, & Lin, 2004; Zhang, Liu, Demchik, Zhai, & Yang, 2004). Artificial LTBR agonist was shown to induce tumor necrosis and decrease tumor burden in vivo in colon cancer or melanoma. (Hu et al., 2013), while recent studies revealed that LTBR mediated tumor progression, triggered by either LTα1b2 or LIGHT stimulation, leads to the recruitment of more infiltrating immune cells and the secretion of pro-survival inflammatory cyto-/chemokines (Ware, 2005). From this, the aim of the project is to compare the signalling changes between WT cells and HOIP absent Hep3B cells using a moTAP tagged LIGHT ligand. This ligand was pulled down by Flag IP, followed by Strep-tactin IP to explore the LTBR signalling complex with and without LUBAC. The result from this experiment would provide an unbiased picture of components of the LTBR-SC, also pointing out the differences between canonical NF-kB pathway and noncanonical Nf-kB pathway.

2025-04-01 | PXD034142 | Pride

Transcriptome profiling of spleen and duodenum upon lymphotoxin beta receptor (LTbR) induction

Project description:To study the effect of LTbR induction on spleen and duodenum transcriptome, we performed RNA sequencing of the spleen and intestine after Intravenous LTbR agonist AC H6 or isotype treatment. We analyzed differential gene expression.

2019-12-31 | GSE126115 | GEO

Transcriptome profiling of spleen and duodenum upon lymphotoxin beta receptor (LTbR) induction

Project description:Transcriptome profiling of spleen and duodenum upon lymphotoxin beta receptor (LTbR) induction

| PRJNA521043 | ENA

LTBR-mediated immunomodulation of the tumor microenvironment promotes anti-tumor responses

Project description:The presence of high endothelial venules (HEV) and tertiary lymphoid structures (TLS) in solid tumors is correlated with favorable prognosis in many cancer types and has been associated with better treatment responses to immune-checkpoint blockade (ICB). However, the molecular mechanisms underlying intratumoral HEV and TLS formation and their contribution to anti-tumor responses remain unclear. Lymphotoxin beta receptor (LTBR) signaling is a critical regulator of lymph node organogenesis and when combined with antiangiogenic and ICB treatment can augment tumor-associated HEV formation. Here we demonstrate that LTBR signaling modulates the tumor microenvironment via multiple mechanisms to promote anti-tumor T cell responses. Systemic activation of the LTBR pathway via agonistic antibody treatment induced tumor-specific HEV formation, upregulated the expression of TLS-related chemokines, and enhanced dendritic cell (DC) and T cell infiltration and activation in syngeneic tumor models. In vitro studies confirmed direct effects of LTBR agonism on DC activation and maturation and associated DC- mediated T cell activation. Single agent LTBR agonist treatment inhibited syngeneic tumor growth in a CD8+ T cell- and HEV-dependent manner; and the LTBR agonist enhanced anti-tumor effects of anti-PD-1 and CAR T cell therapies, respectively. An in vivo tumor screen for TLS-inducing cytokines revealed that the combination of LTBR agonism and lymphotoxin alpha (LT⍺) expression promoted robust intratumoral TLS induction and enhanced tumor responses to anti-CTLA-4 treatment. Collectively, this study highlights crucial functions of LTBR signaling in modulating the tumor microenvironment and inform future HEV/TLS- based strategies for cancer treatments.

2024-08-08 | GSE243170 | GEO

Comparison of gene expression in aorta and CD115+ isolated circulating cells from apoE-/- versus apoE-/-LTbR-/- mice

Project description:Affymetrix Microarrays were used to analyse gene expression in aortas and circulating CD115+ cells of ApoE- and ApoE/Lymphotoxin beta receptor (LTbR)-double-deficent mice fed a Western diet from 8 to 12 weeks of age in order to identify regulated genes and pathways leading to reduced atherosclerosis in ApoE-/-/LTbR-/- mice compared to ApoE-/- littermate controls.

2015-03-16 | GSE63259 | GEO

CD45+ vs CD45- RCC proteome characterization

Project description:Exploration of proteome differences between CD45+ and CD45- cell types in renal cell carcinoma tumors and normal adjacent tissue patient samples.

2020-10-14 | PXD014370 | Pride

Cell circuits between leukemic cells and mesenchymal stem cells block lymphopoiesis by activating lymphotoxin-beta receptor signaling

Project description:Acute lymphoblastic and myeloblastic leukemias (ALL and AML) have been known to modify the bone marrow microenvironment and disrupt non-malignant hematopoiesis. However, the molecular mechanisms driving these alterations remain poorly defined. Here we show that leukemic cells turn-off lymphopoiesis and erythropoiesis shortly after colonizing the bone marrow. ALL and AML cells express lymphotoxin-a1b2 and activate LTbR signaling in mesenchymal stem cells (MSCs), which turns off IL7 production and prevents non-malignant lymphopoiesis. Genetic or pharmacologic disruption of LTbR signaling in MSCs restores lymphopoiesis but not erythropoiesis, reduces leukemic cell growth, and extends survival of transplant recipients significantly. These studies demonstrate that acute leukemias exploit physiological mechanisms governing hematopoietic output as a strategy for gaining competitive advantage. Our studies also reveal that disrupting the cross-talk between leukemia cells and bone marrow niche cells, and specifically the LTbR pathway, offers new therapeutic opportunities.

2023-01-02 | GSE221243 | GEO

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