Transcriptional profile of IL33 & PD1-treated ILC2 from KPC tumor-bearing mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA563328 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10056120.fastq.gz | Fastqsanger.gz | |||
| SRR10056121.fastq.gz | Fastqsanger.gz | |||
| SRR10056122.fastq.gz | Fastqsanger.gz | |||
| SRR10056123.fastq.gz | Fastqsanger.gz | |||
| SRR10056124.fastq.gz | Fastqsanger.gz |
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Project description:We investigated the genetic profiles of IL33 and PD1-treated group 2 innate lymphoid cells (ILC2) harvested from KPC tumors and draining lymph nodes in a pancreatic ductal adenocarcinoma (PDAC) mouse model.
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Project description:We report the RNAseq of mouse pancreatic cancer cell lines with Kras ON vs Kras OFF. TH2 and innate lymphoid cells 2 (ILC2) can stimulate tumor growth by secreting pro-tumorigenic cytokines such as IL4, IL5 and IL13. However, the mechanisms by which type 2 immune cells traffic to the tumor microenvironment (TME) are unknown. Here, in pancreatic ductal adenocarcinoma (PDAC), we show that oncogenic KrasG12D (Kras*) increases the expression of IL33 in cancer cells, which upon secretion recruits and activates the TH2 and ILC2. Correspondingly, cancer cell-specific deletion of IL33 reduces TH2 and ILC2 recruitment and promotes tumor regression. Unexpectedly, we discovered that the cellular release of IL33 into the TME is dependent on the intratumoral fungal mycobiome. Genetic deletion of IL33 or anti-fungal treatment decreases TH2 and ILC2 infiltration and increases survival. Consistent with these murine data, high IL33 expression is observed in approximately 20% of human PDAC, and expression is mainly restricted to cancer cells. These data expand our knowledge of the mechanisms driving PDAC tumor progression and identifies therapeutically targetable pathways involving intratumoral mycobiome-driven secretion of IL33.
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Project description:Our purpose was to analyse the transcriptomic profile of Tregs from tumor-draining lymph nodes of melanoma-bearing mice in order to understand the functional difference between WT and il33-/- Tregs
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Project description:Focal adhesion kinase (FAK) is required for the expression of pro-inflammatory genes that inhibit anti-tumour immunity. Here, we show a novel and crucial role for the dual-function cytokine IL33 in FAK-dependent immune evasion. Specifically, nuclear FAK is required for the expression of IL33, the chemokine Ccl5 and the soluble form of the IL33 receptor, sST2, which are required for evasion of CD8+ T-cell-mediated anti-tumour immunity. Mechanistically, nuclear IL33 associates with FAK and a network of chromatin modifiers and transcriptional regulators, including Taf9, WDR82 and BRD4, while sST2 likely negates effects of IL33 secreted into the tumour microenvironment by infiltrating host immune cells. Finally, protein interaction network analysis implies that nuclear FAK–IL33 complexes impact on transcription factors that regulate NFkB and chemokines like Ccl5 downstream. Our data therefore provide new mechanistic insight into how FAK controls the tumour immune environment via a FAK–IL33/sST2 pathway and demonstrate a novel role for nuclear IL33 downstream of FAK as a component of transcription regulatory complexes that critically modulate anti-tumour immunity.
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Project description:Recently, Bailey et al (2016, Nature) defined four subtypes of pancreatic cancer that are associated with distinct histopathological characteristics and differential survival, namely, Squamous, Pancreatic Progenitor, Immunogenic, and ADEX (Aberrantly Differentiated Endocrine eXocrine). We set out to assess by RNASeq whether loss of CXCR2 was significantly associated with a specific PDAC subtype. Pancreatic tumors were harvested from KPC or KPC Cxcr2-/- mice at endpoint (n=5 v 5), RNA prepared, and RNASeq analysis carried out. Reads were analysed using the bcbio-nextgen framework (https://bcbio-nextgen.readthedocs.org/en/latest/). After quality control and adaptor trimming, reads were aligned to the mouse genome build (UCSC mouse mm10) using STAR. Counts for known genes were generated using the function featureCounts in the R/Bioconductor package \Rsubread\. The R/Bioconductor package edgeR was used to identify differentially expressed genes.
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Project description:ILC2 cells are a newly described cell type whose biology and contribution to disease are poorly understood. ILC2 cells are activated by allergens, viral infection, and/or epithelial damage via IL-33 and IL-25. ILC2 cells require IL-2, IL-7, IL-25 and IL-33 for their survival and expansion. In mice, ILC2s produce multiple mediators primarily associated with type 2 inflammation (IL-13, IL-5, IL-4, IL-6, IL-9, IL-10, GM-CSF, amphiregulin). ILC2 cells may contribute to the pathology of asthma through multiple mediators that include IL-13-independent pathways. Our goal is to compare transcriptional profiles of IL-33- or IL-25-activated ILC2 cells from blood to characterize these cells and to identify marker(s) that can be utilized to detect them in human tissue. ILC2 cells (Lineage negative, CRTH2+, CD161+, CD127+) were purified from human blood of 5 different donors by flow cytometry. The ILC2 yield ranged from 20,000 to 165,000 cells per donor (0.001-0.008% WBC). Purified ILC2s were expanded in vitro in the presence of IL-2, IL-7, IL-33 and IL-25 (each at 50 ng/ml) for 7-10 days. Expanded cells maintained the ILC2 phenotype (Lineage negative, CRTH2+, CD161+, CD127+). The cells were rested for 2 days in the presence of 1 ng/ml IL-2 and IL-7 and then treated in the presence of 1 ng/ml IL-2 and IL-7 with either media control, IL-25 (50 ng/ml), IL-33 (50 ng/ml), and/or TSLP (50 ng/ml) in combination, for 6 or 24 hours. Whole RNA was isolated via the RNeasy kit (Qiagen). Stratagene Universal Human Reference RNA was used as the reference.
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