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

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

PROVIDER: PRJNA521043 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8534020.fastq.gz	Fastqsanger.gz
	SRR8534021.fastq.gz	Fastqsanger.gz
	SRR8534022.fastq.gz	Fastqsanger.gz
	SRR8534023.fastq.gz	Fastqsanger.gz
	SRR8534024.fastq.gz	Fastqsanger.gz

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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

Genome-wide analysis of gene expression in mouse spleen stroma

Project description:Comparison between gene expression profiles of splenic stroma from wild type and lymphotoxin beta receptor knockout mice. The goal was to identify a set of genes which expression in splenic stroma is under lymphotoxin control and which can potentially be important for proper stroma development and function in secondary lymphoid organs. Total RNA isolated from mechanically separated stroma and splenocytes of wild type and LTbR-KO mice, as well as cultured spleen stroma cells from wild type mice. technical replicate - extract: A,B technical replicate - extract: C,D technical replicate - extract: E,F technical replicate - extract: G,H

2013-11-13 | E-GEOD-52294 | biostudies-arrayexpress

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

Transcription profiling of known iron genes in liver, spleen and duodenum of C57BL/6J and SWR mouse strains which have low and high basal iron levels respectively

Project description:Comparison of expression of known 'iron' genes in liver, spleen and duodenum of C57BL/6J and SWR mouse strains which have low and high basal iron levels respectively.

2006-07-11 | E-MEXP-486 | biostudies-arrayexpress

Gene expression data of diagnostic childhood T-ALL samples and human thymocytes

Project description:Lymphotoxin-mediated activation of the lymphotoxin-β receptor (LTβR) has been implicated in several physiological and pathological processes, including lymphoid organ development, T-cell maturation, and solid and hematopoietic malignancies. Its role in T-cell acute lymphoblastic leukemia (T-ALL) or other T-cell malignancies has remained however to be investigated. Here we show that the genes encoding lymphotoxin (LT)-α and LTβ were expressed in T-ALL patient samples, more abundantly in the TAL/LMO molecular subtype, and in the TEL-JAK2 mouse model of cortical/mature T-ALL. Surface LTα1β2 protein was detected in primary mouse T-ALL cells, but only upon phorbol ester stimulation or absence of microenvironmental LTβR interaction. Indeed, in contrast to leukemic cells collected from transplanted Ltbr–/– mice or from co-cultures with Ltbr–/– mouse embryonic fibroblasts (MEF), those collected from Ltbr+/+ mice or from Ltbr+/+ MEF co-cultures presented no surface LT expression. Supporting the notion that LT signaling plays a role in T-ALL, inactivation of the Ltbr gene in mice resulted in a statistically significant delay in TEL-JAK2-induced leukemia onset. Expression of the Lta and Ltb genes was found to be increased at the early asymtptomatic stages of TEL-JAK2 T-ALL, when only low proportions of malignant thymocytes are present in normal sized thymus. Interestingly, young asymptomatic TEL-JAK2;Ltbr–/– mice presented significantly less leukemic thymocytes than TEL-JAK2;Ltbr+/+ mice. Together, these data indicate that early lymphotoxin expression by T-ALL cells activates LTβR signaling in thymic stromal cells, thus promoting leukemogenesis.

2015-11-20 | GSE66638 | GEO

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

Fibroblastic reticular cells in the spleen - bulk RNAseq

Project description:Splenic white pulp (WP) structures are underpinned by fibroblastic stromal cells (FSCs) to facilitate splenic compartmentalization and execute efficient immune responses. Although distinct WP FSCs exhibit various molecular traits, the origin and the hierarchical differentiation of different cell subsets are not characterized. Here we showed, the organization of splenic WP and the differentiation of WP FSCs were governed by lymphotoxin beta receptor (LTβR) signaling pathway. Cell fate mapping analysis revealed that different WP fibroblastic stromal cells descend from a common perivascular LTβR-sensitive mesenchymal lymphoid organizer cells (mLTo) at prenatal stage. Moreover, embryonic mLTo cells required LTβR signaling to give rise to different WP stromal cell subsets, while the proliferation of these cells was devoid of LTβR signaling but followed the development of WP during ontogeny. Moreover, cell fate mapping from different time point indicated a consecutive commitment of mLTo cells initiated from the proximal region around the splenic artery. RNAseq and differentiation trajectory analysis of distinct FSCs showed that Ltbr-deficient cells and perivascular reticular cells (PRCs) from adult spleen exhibited a progenitor phenotype and revealed a closer hierarchical lineage with embryonic mLTo cells. Taken together, our results unveil that embryonic mLTo cells residing in the perivascular niches can give rise to different FSC populations in a LTβR-dependent manner during development.

2019-03-27 | E-MTAB-7097 | biostudies-arrayexpress

insulin resistant duodenum vs. non-insulin resistant duodenum

Project description:insulin resistant duodenum vs. non-insulin resistant duodenum

| PRJNA615363 | ENA

insulin resistant duodenum vs. non-insulin resistant duodenum

Project description:Transcriptional profiling of duodenum from non-obese patients and patients with morbid obesity comparing non-insulin resistance vs. insulin resistande. Goal was to determine the involvement of the duodenum in the development of insulin resistance and the possible influence of obesity.

2022-06-01 | GSE147562 | 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

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