Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells

ABSTRACT: Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells

PROVIDER: PRJNA384189 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5479962.fastq.gz	Fastqsanger.gz
	SRR5479963.fastq.gz	Fastqsanger.gz
	SRR5479993_1.fastq.gz	Fastqsanger.gz
	SRR5479993_2.fastq.gz	Fastqsanger.gz
	SRR5479995_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells [Run2]

Project description:Tissue repair is a subset of a broad repertoire of IL-4/IL-13-dependent host responses during helminth infections. Here, we show that IL-4/IL-13 alone were not sufficient, but IL-4/IL-13 together with apoptotic cells induced the tissue repair program in macrophages. Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and induction of anti-inflammatory/tissue repair genes in the lung following helminth infection or the damage caused by induction of colitis in the gut. In contrast, recognition of apoptotic cells was dispensable for cytokine-dependent induction of pattern recognition receptor, cell adhesion or chemotaxis genes in macrophages. Detection of apoptotic cells can therefore spatially compartmentalize or prevent premature or ectopic activity of pleiotropic, soluble cytokines, such as IL-4/IL-13.

2017-05-11 | GSE98168 | GEO

Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells [Run1]

2017-05-11 | GSE98167 | GEO

Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells.

Project description:Tissue repair is a subset of a broad repertoire of interleukin-4 (IL-4)- and IL-13-dependent host responses during helminth infection. Here we show that IL-4 or IL-13 alone was not sufficient, but IL-4 or IL-13 together with apoptotic cells induced the tissue repair program in macrophages. Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and the induction of anti-inflammatory and tissue repair genes in the lungs after helminth infection or in the gut after induction of colitis. By contrast, the recognition of apoptotic cells was dispensable for cytokine-dependent induction of pattern recognition receptor, cell adhesion, or chemotaxis genes in macrophages. Detection of apoptotic cells can therefore spatially compartmentalize or prevent premature or ectopic activity of pleiotropic, soluble cytokines such as IL-4 or IL-13.

| S-EPMC5556699 | biostudies-literature

Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells

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

2017-05-11 | GSE98169 | GEO

Whole Lung Proteome in N. brasiliensis Infection in IL-13 deficient mice.

Project description:IL-13 plays a key role during protective type 2 immune responses at mucosal sites, such as during infection with nematodes. However, dysregulation of IL-13 can also contribute to the pathogenesis of allergic and fibrotic diseases. Matrix remodelling is an important component of repair processes in the lung but is also a hallmark of chronic diseases such as asthma. Since IL-13 shares receptors and signalling pathways with IL-4, disentangling the relative contributions of these two type 2 cytokines has been challenging. Additionally, little is known about the singular role of IL-13 in more acute settings of tissue injury/repair and whether IL-13 regulates remodelling of the extracellular matrix following tissue injury. In this study, we used Nippostrongylus brasiliensis infection as model of acute lung tissue damage and repair by comparing responses between WT and IL-13-deficient mice, in which IL-4 signalling is intact.

2021-06-11 | PXD021853 | Pride

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

2023-01-31 | GSE218663 | GEO

Innate type 2 immunity controls hair follicle commensalism by Demodex mites [IL-4, IL-13]

Project description:Demodex mites are obligate commensal parasites of hair follicles (HF) in mammals. Normally asymptomatic, inflammatory outgrowth of mites can accompany malnutrition, immune dysfunction and aging, but mechanisms restricting Demodex outgrowth and pathogenesis are not defined. Here, we show that control over mite HF colonization of mice requires ILC2s, IL-13, and its receptor IL-4Ra, but not IL-4 or the adaptive immune system. Epithelial HF-associated ILC2s elaborate IL-13 that attenuates HF and epithelial cell proliferation at anagen onset; in their absence, Demodex colonization leads to increased epithelial proliferation and replacement of gene programs for repair by aberrant inflammatory programs leading to loss of barrier function and premature HF exhaustion over time. Humans with rhinophymatous acne rosacea, a nasal inflammatory condition associated with a high burden of Demodex, had increased HF inflammatory cells with decreased type 2 cytokines, consistent with the inverse relationship seen in mice. Our studies uncover a critical role for skin ILC2s and IL-13, which comprise an immune checkpoint necessary to sustain cutaneous integrity and restrict pathologic infestation by colonizing HF mites.

2022-11-29 | GSE198657 | GEO

Mus musculus

Project description:Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells [Run1]

| PRJNA384186 | ENA

Mus musculus

Project description:Macrophage function in tissue repair and remodeling requires IL-4/IL-13 with apoptotic cells [Run2]

| PRJNA384200 | ENA

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

| PRJNA904774 | ENA