Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dysfunction of S100A4+ effector memory CD8+ T cells aggravates asthma

ABSTRACT: Dysfunction of S100A4+ effector memory CD8+ T cells aggravates asthma

PROVIDER: PRJNA680609 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13130500_1.fastq.gz	Fastqsanger.gz
	SRR13130500_2.fastq.gz	Fastqsanger.gz
	SRR13130501_1.fastq.gz	Fastqsanger.gz
	SRR13130501_2.fastq.gz	Fastqsanger.gz
	SRR13130502_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Dysfunction of S100A4+ effector memory CD8+ T cells aggravates asthma

Project description:Progressive loss of effector functions, especially IFN-γ secreting capability, in effector memory CD8+ T (CD8+ TEM) cells plays a causal role in asthma worsening. However, the mechanisms of CD8+ TEM cell dysfunction remain elusive. Here, we report that S100A4 drives CD8+ TEM cell dysfunction, impairing their protective memory response and promoting asthma worsening in OVA-induced asthma model. We find that allergic CD8+ TEM cells contain two subsets based on S100A4 expression. S100A4+ subsets exhibit dysfunctional effector phenotypes with increased proliferative capability, whereas S100A4- subsets retain effector function but are more inclined to apoptosis, giving rise a dysfunctional CD8+ TEM cell pool. Mechanistically, S100A4 upregulation of mitochondrial metabolism results in a decrease of acetyl-CoA levels, which impair the transcription of effector genes, especially ifn-γ, facilitating cell survival, tolerance and memory potential. Our findings thus reveal general insights into how S100A4 reprograms CD8+ TEM cells into dysfunctional and less protective phenotypes to promote asthma worsening.

2022-03-11 | GSE162116 | GEO

METTL3 Deficiency in Macrophage Aggravates Neutrophilic Asthma by Regulating ZBP1-NLRP3 Inflammasome Activation

Project description:N6-methyladenosine (m6A), the most abundant RNA modification, plays the essential role in the immune disorders. Yet, the role of m6A and its master regulator, methyltransferase-like 3 (METTL3) in asthma remain ambiguous. Here, we found that macrophage deficient in METTL3 aggravates the ovalbumin/lipopolysaccharide (OVA/LPS)-induced neutrophilic asthma. Subsequently, we observed that METTL3 deficiency facilitates NLRP3 but not AIM2 and NLRC4-dependent inflammasome activation and IL-1β secretion. Mechanistically, METTL3 deficiency enhanced NLRP3 inflammasome activation were dependent on upregulation of ZBP1 and TRAF1. Lastly, we elucidated that METTL3 negatively regulates ZBP1 expression through m6A modification dependence. In summary, the study unveils the function of m6A in regulating NLRP3 inflammasome activation in macrophage and identifies potential targets in therapeutic intervention of neutrophilic asthma.

2025-02-09 | GSE283939 | GEO

Macrophagic S100A4 drives macrophage protumor activation and promotes tumor growth through controlling PPAR-γ induction

Project description:The lipid-metabolism up-regulation-mediated M2 polarization provides tumor-associated macrophages (TAMs) with protumor phenotypes during tumor development and progression. However, how TAMs reprogram their lipid-metabolism responding to M2 activators remains unclear. Here, we report that S100A4 is a determinant of macrophage M2 polarization. We find that the growth of carcinoma grafts was impaired in myeloid S100A4-deficient mice. Coincidentally, ablating S100A4 in macrophages reduced their capability of macrophage into utilization utilize of exogenous fatty acids as their major energy source for oxidation. Mechanistic analysis demonstrates that the induction of PPAR-γ responding to Th2 cytokine, IL-4, was halted in s100a4-deleted TAMs, as well as in bone marrow-derived macrophages, and as well as in Raw264.7 cells. Further molecular analyses reveal that CD36, downstream from S100A4-PPARγ, is the major effector for lipid uptake of S100A4+ macrophages. FurthermoreImportantly, higher levels of S100A4 is closely associated with tumor resistance to chemotherapy in murine models as well as poor prognosis of cancer patients in clinic . Our study thus suggests that blocking S100A4 constitutes a treatment strategy to reprogram macrophages toward an antitumor state by inhibiting PPAR-γ-induction mediated gene up-regulation.

2021-06-30 | GSE161060 | GEO

S100A4+ Stromal Cells from Normal Lung vs. Metastatic Lung

Project description:Analysis of S100A4+ stromal cells at the gene expression level in physiological setting versus metastatic setting. Total RNA was isolated from FACS-sorted S100A4+ stromal cells from normal lung of S100A4-GFP transgenic mice compared to FACS-sorted S100A4+ stromal cells from metastatic lung of 4T1 tumor-bearing S100A4-GFP transgenic mice.

2011-08-29 | E-GEOD-31711 | biostudies-arrayexpress

Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction

Project description:Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction

| PRJNA792555 | ENA

Comparison of gene expression profiles between S100A4-positive and -negative cells isolated from the Peyer's patches

Project description:To identify gene products expressed in S100A4-producing cells in Peyer's patches, we used transgenic mice expressing enhanced green fluorescent protein (EGFP) under the control of the mouse S100A4 promoter (S100A4-GFP mice) and analyzed gene expression profiles using microarray. As a result, we found that S100A4-producing cells expressed many genes characteristic of LysoMac/DCs and ILC3s.

2019-10-22 | GSE127686 | GEO

Neuronal ABCA7 deficiency aggravates mitochondrial dysfunction and neurodegeneration in Alzheimer’s disease

Project description:Neuronal ABCA7 deficiency aggravates mitochondrial dysfunction and neurodegeneration in Alzheimer’s disease

| PRJNA1231531 | ENA

Differential gene expression profile of S100A4 null mouse lens

Project description:Whole lens transcriptome profiling by RNA-seq analysis was performed to investigate the role of S100A4 in lens architecture and function. These studies yielded the intriguing discovery that absence of S100A4 in the lens results in robust induction of gene expression of S100A5, an olfactory sensory neuron specific protein, and of genes encoding various photoreceptor and Müller glial cell proteins

2020-01-19 | GSE143909 | GEO

S100A4+ Stromal Cells from Normal Lung vs. Metastatic Lung

Project description:Analysis of S100A4+ stromal cells at the gene expression level in physiological setting versus metastatic setting.

2011-08-30 | GSE31711 | GEO

METTL3 Deficiency in Macrophage Aggravates Neutrophilic Asthma by Regulating ZBP1-NLRP3 Inflammasome Activation

Project description:METTL3 Deficiency in Macrophage Aggravates Neutrophilic Asthma by Regulating ZBP1-NLRP3 Inflammasome Activation

| PRJNA1196358 | ENA