Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Long-term repopulation of Langerhans cell network following immune injury is inefficient and solely dependent upon influx of monocyte precursors

ABSTRACT: Long-term repopulation of Langerhans cell network following immune injury is inefficient and solely dependent upon influx of monocyte precursors

PROVIDER: PRJNA534470 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8949950_1.fastq.gz	Fastqsanger.gz
	SRR8949950_2.fastq.gz	Fastqsanger.gz
	SRR8949960_1.fastq.gz	Fastqsanger.gz
	SRR8949960_2.fastq.gz	Fastqsanger.gz
	SRR8949951_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 42

Similar Datasets

Long-term repopulation of Langerhans cell network following immune injury is inefficient and solely dependent upon influx of monocyte precursors

Project description:RNAseq gene expression following the repopulation of the langerhans cell network in immune deficient irradiated mice after ectopic injection of donor bone marrow cells

2019-06-14 | GSE130257 | GEO

Expression data of Langerhans cells purified from Il34+/LacZ and Il34LacZ/LacZ mice after UV treatment

Project description:We examined the impact of IL-34 on repopulation of Langerhans cells after inflammation Langerhans cells were FACS-purified from Il34+/LacZ and Il34LacZ/LacZ mice after UV treatment

2015-11-04 | E-GEOD-74686 | biostudies-arrayexpress

Expression data of Langerhans cells purified from Il34+/LacZ and Il34LacZ/LacZ mice after UV treatment

Project description:We examined the impact of IL-34 on repopulation of Langerhans cells after inflammation

2015-11-04 | GSE74686 | GEO

Langerhans cell RNAseq

Project description:Langerhans cell RNAseq

| PRJNA587425 | ENA

MiR-23a Regulates Skin Langerhans Cell Phagocytosis and Inflammation-Induced Langerhans Cell Repopulation.

Project description:Langerhans cells (LCs) are skin-resident macrophage that act similarly to dendritic cells for controlling adaptive immunity and immune tolerance in the skin, and they are key players in the development of numerous skin diseases. While TGF-β and related downstream signaling pathways are known to control numerous aspects of LC biology, little is known about the epigenetic signals that coordinate cell signaling during LC ontogeny, maintenance, and function. Our previous studies in a total miRNA deletion mouse model showed that miRNAs are critically involved in embryonic LC development and postnatal LC homeostasis; however, the specific miRNA(s) that regulate LCs remain unknown. miR-23a is the first member of the miR-23a-27a-24-2 cluster, a direct downstream target of PU.1 and TGF-b, which regulate the determination of myeloid versus lymphoid fates. Therefore, we used a myeloid-specific miR-23a deletion mouse model to explore whether and how miR-23a affects LC ontogeny and function in the skin. We observed the indispensable role of miR-23a in LC antigen uptake and inflammation-induced LC epidermal repopulation; however, embryonic LC development and postnatal homeostasis were not affected by cells lacking miR23a. Our results suggest that miR-23a controls LC phagocytosis by targeting molecules that regulate efferocytosis and endocytosis, whereas miR-23a promotes homeostasis in bone marrow-derived LCs that repopulate the skin after inflammatory insult by targeting Fas and Bcl-2 family proapoptotic molecules. Collectively, the context-dependent regulatory role of miR-23a in LCs represents an extra-epigenetic layer that incorporates TGF-b- and PU.1-mediated regulation during steady-state and inflammation-induced repopulation.

| S-EPMC10376168 | biostudies-literature

Langerhans cell RNAseq

Project description:CD45.1 bone marrow cells were transplanted into irradiated CD45.2 host to generate bone marrow chimera mice. Skin langerhans cells and other dendritic cell subsets were sorted from chimera mice and sequenced.

2021-03-22 | GSE139877 | GEO

Notch is active in Langerhans Cell Histiocytosis and confers pathognomonic features on dendritic cells.

Project description:Langerhans cell histiocytosis (LCH) is a disease characterized by the accumulation of eponymous CD1a+ Langerin+ Langerhans-cell (LC)-like dendritic cells (DC) of largely unknown origin. Here we have performed comparative transcriptome analysis of highly purified CD207+/CD1a+ Langerhans cell histiocytosis (LCH) cells derived from different locations and disease courses and three major human dendritic cell lineages: epidermal Langerhans cells, myeloid dendritic cells (mDC1) and plasmacytoid dendritic cells (pDC) in order to investigate the relationship between LCH cells and naturally occurring dendritic cells. Data obtained indicate that LCH cells form a distinct DC entity. Furthermore, we have identified transcripts that are uniquely expressed by LCH cells in comparison to LC, mDC1, and pDC, and induce LCH-specific features in human DC. Primary cells were isolated from peripheral blood (mDC1 and pDC), skin (epidermal Langerhans cells) and CD207+/CD1a+ Langerhans cell histiocytosis (LCH) cells derived from different locations. RNA was isolated from these cells ex vivo.

2012-10-24 | E-GEOD-35340 | biostudies-arrayexpress

Langerhans dendritic cell differentiation and TGFbeta

Project description:To identify genes with a potential role in Langerhans dendritic cell differentiation, progenitor cells from human cord blood were analyzed by Affymetrix GeneChip U133Plus 2.0 microarray profiling

2016-12-31 | GSE31318 | GEO

Aberrant calcium influx causes fiber type shift and mitochondrial loss in skeletal muscle

Project description:Skeletal muscle excitation-contraction (EC) coupling is independent of calcium influx. In fact alternative splicing of the voltage-gated calcium channel CaV1.1 actively suppresses calcium currents in mature muscle. Why this might be necessary is not known. However, splicing defects causing aberrant expression of the calcium-conducting embryonic CaV1.1e splice variant correlate with muscle weakness in myotonic dystrophy. Here we deleted CaV1.1 exon 29 in mice. The continued expression of CaV1.1e resulted in increased calcium influx during EC coupling and spontaneous calcium sparks. While overall motor performance was normal, muscle force was reduced, endurance enhanced, and the fiber type composition shifted toward slower fibers. In contrast, oxidative enzyme activity and the mitochondrial content declined. Together with the dysregulation of key regulators of the slow program these findings indicate that limiting calcium influx during skeletal muscle EC coupling is important for the calcium signalâs secondary function in the activity-dependent regulation of fiber type composition. Differential gene expression between soleus and EDL muscle fibres from wildtype and Cav1.1 delta E29 mice.

2016-04-01 | E-GEOD-67803 | biostudies-arrayexpress

The RNA sequencing of brain after microglial depletion and repopulation

Project description:The RNA sequencing of brain after microglial depletion and repopulation

2018-02-24 | GSE108269 | GEO