Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Development of Fit Epidermal Resident Memory T Cells Requires Antigen Encounter in the Skin

ABSTRACT: Development of Fit Epidermal Resident Memory T Cells Requires Antigen Encounter in the Skin

PROVIDER: PRJNA1196360 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31665389.fastq.gz	Fastqsanger.gz
	SRR31665390.fastq.gz	Fastqsanger.gz
	SRR31665391.fastq.gz	Fastqsanger.gz
	SRR31665392.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Development of Fit Epidermal Resident Memory T Cells Requires Antigen Encounter in the Skin

Project description:CD8+ tissue resident memory T cells (TRM) develop from effectors that are recruited into peripheral tissues by infection or inflammation where they persist and provide defense against subsequent challenges. Long-term persistence of epidermal TRM requires autocrine TGFβ that is transactivated by integrins expressed on keratinocytes. In response to inflammation, the availability of TGFβ transactivation is limited. Antigen-experienced TRM that encountered antigen in the epidermis during their development are more fit and outcompete bystander TRM for TGFβ transactivation resulting in their enrichment in the epidermis. Transcriptomic analysis of endogenous epidermal TRM revealed that antigen-experienced TRM were enriched for TRM signature genes while bystander TRM retained the transcriptome of an earlier developmental state. Following antigen recall, antigen-experienced TRM displayed accelerated proliferation kinetics compared with bystanders that was determined by the TCR signal-strength during their differentiation the skin. Finally, antigen experienced TRM expressed TGFβRIII, which increases avidity of the TGFβRI/II receptor complex. Selective ablation of Tgfbr3 from antigen experienced TRM reduced their capacity to persist when TGFβ activation was limited thus rendering them phenotypically like bystander TRM. In sum, antigen-driven TCR signaling in the epidermis during TRM differentiation represents a required final step in ontogeny resulting in a lowered requirement on TGFβ transactivation for persistence and increased proliferation during recall responses that together result in the enhanced fitness of antigen-experience epidermal TRM.

2024-12-10 | GSE283941 | GEO

Fe-FIT-Diff

Project description:au13-06_fit - Fe-FIT-Diff - FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) is a regulator of Fe deficiency responses in the root. FIT is a basic helix-loop-helix protein. Here, we investigated the transcriptome changes in response to Fe deficiency (- Fe) versus the control condition (+ Fe) in wild type, the fit-3 loss of function mutant and in FIT overexpression plants.

2015-02-14 | GSE65934 | GEO

Antigen-specific and bystander epidermal CD8+ resident memory T cells

Project description:Antigen-specific and bystander epidermal CD8+ resident memory T cells

| PRJNA658649 | ENA

fe-fit-diff_6d-Differential gene expression in A. thaliana roots depending on iron supply and FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) abundance

Project description:au15-01_iron-fit - fe-fit-diff_6d - Changes in gene expression profiles between fit knock-out, wild-type and FIT overexpressor seedlings under sufficient iron supply and under iron deficiency. - Col-0, HA-FIT and fit-3.

2016-07-01 | GSE80281 | GEO

fe-fit-diff_6d-Differential gene expression in A. thaliana roots depending on iron supply and FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) abundance

2016-07-01 | E-GEOD-80281 | biostudies-arrayexpress

The establishment of resident memory B cells in the lung requires local antigen encounter.

Project description:Memory B cells are found in lymphoid and non-lymphoid tissues, suggesting that some may be tissue-resident cells. Here we show that pulmonary influenza infection elicited lung-resident memory B cells (BRM cells) that were phenotypically and functionally distinct from their systemic counterparts. BRM cells were established in the lung early after infection, in part because their placement required local antigen encounter. Lung BRM cells, but not systemic memory B cells, contributed to early plasmablast responses following challenge infection. Following secondary infection, antigen-specific BRM cells differentiated in situ, whereas antigen-non-specific BRM cells were maintained as memory cells. These data demonstrate that BRM cells are an important component of immunity to respiratory viruses such as influenza virus and suggest that vaccines designed to elicit BRM cells must deliver antigen to the lungs.

| S-EPMC6392030 | biostudies-literature

Sweat gland development requires an eccrine dermal niche and couples two epidermal programs

Project description:Eccrine sweat glands are indispensable for human thermoregulation and, similar to other mammalian skin appendages, form from multipotent epidermal progenitors. Limited understanding of how epidermal progenitors specialize to form these vital organs has precluded therapeutic efforts toward their regeneration. Herein, we applied single-nucleus transcriptomics to compare the expression content of wild-type, eccrine-forming mouse skin to that of mice harboring a skin-specific disruption of Engrailed 1 (En1), a transcription factor that promotes eccrine gland formation in humans and mice. We identify two concurrent but disproportionate epidermal transcriptomes in the early eccrine anlagen: one that is shared with hair follicles and one that is En1 dependent and eccrine specific. We demonstrate that eccrine development requires the induction of a dermal niche proximal to each developing gland in humans and mice. Our study defines the signatures of eccrine identity and uncovers the eccrine dermal niche, setting the stage for targeted regeneration and comprehensive skin repair.

2023-11-10 | GSE220977 | GEO

RNA sequencing of resident epidermal populations at steady state and following UV challenge

Project description:Purpose: to characterise the steady state gene expression and transcriptomic response of resident murine epidermal immune cells (dendritic epidermal T cells, DETC; Langerhans cells, LCs) and epithelial cells (interfollicualr keratinocytes) to non-microbial stress in the form of ultraviolet B (UVB) radiation Methods: 6 C57Bl/6 mice were administered 300mJ/cm^2 UVB radiation to the dorsal side of both ears 24hr prior to tissue harvest, and another 6 administered the same dose 4 hr prior. Ears were harvested and dorsal and ventral ear sheets were separated. Samples were pooled from 2 mice to generate 3 biological replicates per timepoint. Dorsal sheets were used for UV samples, while ventral sheets from 24hr UV mice were used as unchallenged skin. Epidermis was separated and digested, and epidermal populations were FACS sorted. Libraries were prepared and sequenced on an Illumina HiSeq 2500. Conclusions: these data reveal the transcriptomic response of LC, DETC and interfollicular keratinocytes to acute epithelial stress in the form of DNA damage

2021-12-12 | GSE160477 | GEO

Sweat gland development requires an eccrine dermal niche and couples two epidermal programs

Project description:Sweat gland development requires an eccrine dermal niche and couples two epidermal programs

| PRJNA912194 | ENA

Epidermal Stratification Requires Retromer-Mediated Desmoglein-1 Recycling

Project description:Sorting transmembrane cargo is essential for tissue development and homeostasis. However, mechanisms of intracellular trafficking in stratified epidermis are poorly understood. Here we identify an interaction between the retromer endosomal trafficking component, VPS35, and the desmosomal cadherin, Desmoglein-1 (Dsg1). Dsg1 is specifically expressed in stratified epidermis and when properly localized on the plasma membrane of basal keratinocytes, promotes stratification. We show that the retromer drives Dsg1 recycling from the endo-lysosomal system to the plasma membrane to support stratification. The retromer-enhancing chaperone, R55, promotes the membrane localization of Dsg1 and a trafficking-deficient mutant associated with a severe inflammatory skin disorder, enhancing its ability to promote stratification. In the absence of Dsg1, retromer association with and expression of the glucose transporter GLUT1 increases, exposing a potential link between Dsg1 deficiency and epidermal metabolism. Our work provides the first evidence for retromer function in epidermal regeneration, identifying it as a potential therapeutic target.

2023-07-24 | PXD036646 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data