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Kidney-resident CD8 T cells downregulate IL-18R during maturation

ABSTRACT: Kidney-resident CD8 T cells downregulate IL-18R during maturation

PROVIDER: PRJNA438210 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6831600.fastq.gz	Fastqsanger.gz
	SRR6831601.fastq.gz	Fastqsanger.gz
	SRR6831602.fastq.gz	Fastqsanger.gz
	SRR6831597.fastq.gz	Fastqsanger.gz
	SRR6831598.fastq.gz	Fastqsanger.gz

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Kidney-resident CD8 T cells downregulate IL-18R during maturation

Project description:Using the expression of IL-18 receptor (CD218) as a surface marker, CD69+ kidney-resident CD8 T cells can be separated into two subsets. Transcriptional analysis suggests that IL-18R low subset represents the mature tissue-resident T cells

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Regulatory T cells Maintain Lung Function Upon Infectious Damage

Project description:RNA-Seq analysis of Treg cell subsets isolated from lungs of Il10GFPFoxp3Thy1.1 mice. Thy1.1+ Treg cells were FACS-sorted into IL-10–IL-18R–, IL-10+IL-18R– and IL10–IL-18R+ populations on day 5 following intranasal infection with 0.5 LD50 PR8-OTI influenza virus. mRNA profiles of each Thy1.1+ Treg cell population (IL-10–IL-18R–, IL-10+IL-18R– and IL10–IL-18R+) from lungs on day 5 following influenza infection from 5 infected mice, sorted into TRIzol LS reagent.

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Noncanonical Il-1β maturation in microglia impairs cognition in chronic kidney disease via neuronal IL1R signaling

Project description:While cognitive impairment is common in peripheral diseases such as chronic kidney disease (CKD), mechanistic insights and effective therapies are lacking. Here, we show that microglial potassium (K+) dyshomeostasis induces noncanonical IL-1β maturation and neuronal dysfunction via IL-1R signaling in CKD. Despite inflammasome activation in the brain, microglial caspase-1 deficiency does not improve inflammation and cognition in CKD mice. Noncanonical IL-1β maturation in microglia is mediated by the cathepsin C–caspase-8 pathway. Restoring K+ homeostasis in microglia or genetically inhibiting neuronal IL-1R1 signaling abolishes CKD-induced cognitive impairment. Microglial K+ dyshomeostasis and noncanonical microglial IL-1β maturation may therefore be druggable targets in some forms of cognitive impairment. These insights identify a new intercellular microglia–neuron crosstalk and identify potential therapeutic targets to combat inflammasome-induced neuronal dysfunction.

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IL-18R signaling affects transcriptional profile of intratumoral CTLs

Project description:We report that intratumoral IL-18R-deficient T cells show decreased T cell exhaustion in a murine pancreatic cancer model

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Regulatory T cells Maintain Lung Function Upon Infectious Damage

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Mouse resident lung eosinophils are dependent on IL-5

Project description:Mouse resident lung eosinophils are dependent on IL-5

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Tissue resident iNKT17 cells facilitate cancer cell extravasation in liver metastasis via IL-22

Project description:The crosstalk among the immune system, cancer cells and the tissue microenvironment is fundamental for the emergence of organ-specific niches that facilitate metastasis formation. Here, we studied the involvement of IL-22, which is known to be produced by immune cells and to act on the tissue, in mediating this crosstalk and thus metastasis formation. We found that Il22-deficient mice and mice treated with an IL-22 antibody are protected from liver and lung metastasis formation, while over expression of IL-22 promoted metastasis formation. Mechanistically, IL-22 acted on endothelial cells thereby promoting endothelial permeability and cancer cell transmigration via induction of endothelial aminopeptidase N. Finally, tissue resident iNKT17 cells were the key source of IL-22 in the liver. Thus, targeting tissue resident immune cells derived IL-22 represents a potential therapeutic target in metastasis formation.

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Mouse resident lung eosinophils are dependent on IL-5

Project description:Purpose: we aimed to characterized eosinophils in the murine model of asthma Methods: Eosinophils were sorted from the lung of naïve and and HDM-induced asthma mice. There after RNA was extracted from the sorted eosinophils and subjected to RNAseq. Results:we demonstrated that resident lung eosinophils require IL-5 for their survival and that the expression of Siglec-F, is regulated by IL-5 . Conclusion: Our data suggest that the distinct eosinophil populations in the asthmatic lung represent a continuum of activation states rather than distinct eosinophil subsets.

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IL-18R signaling affects transcriptional profile of intratumoral CTLs

Project description:IL-18R signaling affects transcriptional profile of intratumoral CTLs

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Changes in bone marrow resident monocyte gene expression upon induction of ischemia

Project description:There is considerable interest in the potential of cell-based approaches to mediate therapeutic angiogenesis for acute and chronic vascular syndromes. Using a mouse model of HLI, we showed previously that adoptive transfer of a small number of donor monocytes enhanced revascularization significantly. Herein, we provide data suggesting that the BM resident monocytes sense systemic signals that influence their future functional capacity. Specifically, following induction of distant ischemia, the angiogenic capacity of BM resident monocytes is reduced markedly. We provide evidence that G-CSF and IL-6 represent such conditioning signals. Systemic levels of G-CSF and IL-6 are increased significantly following induction of HLI. Accordingly, BM resident monocytes from ischemic mice exhibited increased pSTAT3 and STAT3 target gene expression. Finally, G-CSFR(-/-) and IL-6(-/-) mice were resistant to the deleterious effects of ischemic conditioning on monocyte angiogenic potential. RNA expression profiling suggested that ischemia-conditioned monocytes in the BM up-regulate the well-described M2 polarization markers Chi3l4 and Lrg1. Consistent with this observation, M2-skewed monocytes from SHIP(-/-) mice also had impaired angiogenic capacity. Collectively, these data show that G-CSF and IL-6 provide signals that determine the angiogenic potential of BM resident monocytes. Bone marrow was harvested from CX3CR1+/GFP heterozygous mice and CX3CR1-GFP+ monocytes were sorted at baseline and at 24 hours post-induction of hindlimb ischemia by femoral artery ligation. Paired samples from three independent experiments were analyzed.

2010-04-26 | E-GEOD-21509 | biostudies-arrayexpress

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