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IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2 [bulk rnaseq]

ABSTRACT: IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2 [bulk rnaseq]

PROVIDER: PRJNA750052 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15258471_1.fastq.gz	Fastqsanger.gz
	SRR15258471_2.fastq.gz	Fastqsanger.gz
	SRR15258472_1.fastq.gz	Fastqsanger.gz
	SRR15258472_2.fastq.gz	Fastqsanger.gz
	SRR15258473_1.fastq.gz	Fastqsanger.gz

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IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2

Project description:IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2

| PRJNA750059 | ENA

IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2 [bulk rnaseq]

Project description:Aging impairs the integrated immunometabolic responses which have evolved to maintain core body temperature in homeotherms to survive cold-stress, infections, and dietary restriction. Adipose tissue inflammation regulates the thermogenic stress response but how adipose tissue-resident cells instigate thermogenic failure in the aged are unknown. Here, we define alterations in the adipose-resident immune system and identify that type 2 innate lymphoid cells (ILC2) are lost in aging. Restoration of ILC2 numbers in aged mice to levels seen in adults through IL-33 supplementation failed to rescue old mice from metabolic impairment and increased cold-induced lethality. Transcriptomic analyses revealed intrinsic defects in aged ILC2, and adoptive transfer of adult ILC2 are sufficient to protect old mice against cold. Thus, the functional defects in adipose ILC2 during aging drive thermogenic failure.

2021-07-29 | GSE180858 | GEO

IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2 [single cell rnaseq]

2021-07-29 | GSE180910 | GEO

IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2 [single cell rnaseq]

Project description:IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2 [single cell rnaseq]

| PRJNA750058 | ENA

IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-29 | GSE180911 | GEO

Human ILC2 cells stimulated with IL-25, IL-33, or TSLP

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.

2013-12-31 | E-GEOD-45458 | biostudies-arrayexpress

Human ILC2 cells stimulated with IL-25, IL-33, or TSLP

2013-12-31 | GSE45458 | GEO

Role of IL-33/ILC2 in bladder infection

Project description:The impact of IL-33 on urinary tract infections (UTI) was assessed by comparing Il33KO mice with wild-type (WT) mice within the bladder;The effect of ILC2 on UTI was assessed by comparing Il5cre+/DTA+ mice with WT mice within the bladder.

2024-10-20 | GSE259362 | GEO

Homeostatic leukotrienes, IL-25, and IL-33 signals on intestinal ILC2 status

Project description:We report the high-throughput profiling of murine intestinal type 2 innate lymphoid cells (ILC2) transcriptome. By obtaining over 8.7 million bases of sequence, we generated genome-wide expression maps of mouse ILC2 without the presense of known activation signals(IL-25, IL-33 receptor) and new non-redundant signal (leukotriene). We find that homeostatic signaling minimally contributes to intestinal ILC2 activation statu. 500 ILC2s were sorted as CD45+Lineage-IL-17RB+

2020-02-16 | GSE144956 | GEO

Expression data of ILC2 cells from Ets1-deleted and littermate control mice

Project description:The ETS1 transcription factor is required for the development and cytokine-induced expansion of ILC2 ILC2 cells isolated from ETS1-deleted or litter mate control mice were cultured on OP9-DL1 with IL-7 and IL-33. Subsequently, RNA from ICOS+ cells was extracted, labelled and hybridized to Affymetrix microarrays. The goal of this study is to investigate ETS1-dependent genes in developing ILC2 cells.

2016-04-01 | E-GEOD-79742 | biostudies-arrayexpress

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