Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Immunological Proteome Resource (ImmPRes): Liver derived CD4+ T cell proteomes

ABSTRACT: T cells play a critical role in liver immunity and take part both in the initiation and in the resolution of intrahepatic inflammation. The liver contains conventional CD4 T cells, and Natural Killer T (NKT) cells that express an invariant Vα14 T cell receptor that recognizes glycolipid/CD1d antigen complexes (iNKTs) and play a role in immune surveillance and immune homeostasis. ImmPRes includes a TMT based dataset characterising the proteomes of ex-vivo liver derived CD4+ T cells along with invariant NKT (iNKT) cells

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): T Cell, Liver

SUBMITTER: Alejandro Brenes

LAB HEAD: Doreen A. Cantrell

PROVIDER: PXD036319 | Pride | 2022-08-26

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	PT7381-1.raw	Raw
	PT7381-10.raw	Raw
	PT7381-11.raw	Raw
	PT7381-12.raw	Raw
	PT7381-13.raw	Raw

Items per page:

1 - 5 of 238

Similar Datasets

Defining the T cell proteome and the role of mTORC1 during differentiation using quantitative proteomics

Project description:High-resolution quantitative mass-spectrometry reveals similarities and disparities in how murine naïve CD4 and CD8 T cells respond to immune activation and re-structure proteomes as they differentiate to effector cells. The data map core transcriptional, metabolic and protein synthesis machinery, nutrient transporters and environment sensing molecules and reveal differences in the biosynthetic capacity of CD4 and CD8 T cells. One key nutrient sensing kinase is mammalian target of rapamycin complex1 (mTORC1). The current study identifies common and distinct mTORC1 regulated processes and divergent outcomes of mTORC1 inhibition in naïve versus effector CD4 and CD8 T cell populations. The data provide a resource that maps how immune activation and mTORC1 reshape CD4 and CD8 T cell proteomes and highlights that a deep understanding of T cell phenotype requires modelling of the impact of immune regulators on protein copy number, cellular protein concentrations and the subunit stoichiometry of key protein complexes.

2019-03-28 | PXD012058 | Pride

Tissue adaptation is the dominant driver of the proteomic landscape of intestinal intraepithelial lymphocytes

Project description:Intestinal intraepithelial T lymphocytes (T-IEL) patrol the single layer of epithelial cells lining the gut, and consist of both induced T-IEL, derived from systemic antigen-experienced lymphocytes, and natural IEL, that are developmentally targeted to the intestine. To gain functional insights into these enigmatic cells, we used high-resolution quantitative mass spectrometry to investigate the proteomic landscape of the main T-IEL populations in the gut. Comparing the proteomes of induced T-IEL, tissue-resident memory TCRαβ+ CD8αβ+ cells and natural TCRγδ+ CD8αα+ and TCRαβ+ CD8αα+ T-IEL, with naive CD8+ T cells from lymph nodes reveals striking similarities between T-IEL subsets and the dominant effect of the gut environment on T-IEL phenotypes. Analysis of copy numbers/cell of >7000 proteins provides new understanding of the differences in composition of T cell antigen receptor signal transduction pathways in T-IEL versus conventional T cells and reveals skewing of the metabolic machinery towards an exhausted T cell phenotype adapted to the intestinal environment. This study provides a resource for exploring and understanding how multiple inputs are integrated into T-IEL function.

2021-03-15 | PXD023140 | Pride

Immunological Proteome Resource (ImmPRes): Part two

Project description:Second dataset release from the Immunological Proteome Resource (ImmPRes). This dataset contains both lymphoid and myeloid populations. The whole list is as follows: Bone marrow derived eosinophils, bone marrow derived mast cells, bone marrow derived macrophages, NK cells, TH2 cells, TH17 cells, Cytotoxic T cells cultured in IL15 and Naive CD8+ T cells extractred from the lymph nodes of C57BL/6J mice.

2020-07-02 | PXD020091 | Pride

Immunological Proteome Resource (ImmPRes): Hypoxia dataset

Project description:Third dataset release from the Immunological Proteome Resource (ImmPRes). This dataset contains the study focussing on the effect of Hypoxia in Cytotoxic CD8+ Lymphocytes.

2021-11-03 | PXD020041 | Pride

Super-killer CTLs are generated by single gene deletion of Bach2

Project description:Bach2 codes for a transcriptional regulator exerting major influences on T cell mediated immune regulation. Effector CTLs derived from in vitro activation of murine CD8+ T cells showed increased proliferative and cytolytic capacity in the absence of BACH2. Before activation, BACH2-deficient CD8+ T cells had a higher abundance of memory and reduced abundance of naïve cells compared to wild-type. CTLs derived from central memory T cells were more potently cytotoxic than those derived from naïve T cells, but even within separated subsets, BACH2-deficiency conferred a cytotoxic advantage. Immunofluorescence and electron microscopy revealed larger granules in BACH2-deficient compared to wild-type CTLs, and proteomic analysis showed an increase in granule content, including perforin and granzymes. Thus, the enhanced cytotoxicity observed in effector CTLs lacking BACH2 arises not only from differences in their initial differentiation state but also inherent production of enlarged cytolytic granules. These results demonstrate how a single gene deletion can produce a CTL super-killer.

2022-09-02 | PXD036457 | Pride

Lack of phosphatidylinositol 3-kinase VPS34 in regulatory T cells leads to a fatal lymphoproliferative disorder without affecting their development

Project description:Regulatory T (Treg) cells are essential for the maintenance of immunological tolerance, yet the molecular components required for their maintenance and effector functions remain incompletely defined. Inactivation of VPS34 in Treg cells led to an early, lethal phenotype, with massive effector T cell activation and inflammation, like mice lacking Treg cells completely. However, VPS34-deficient Treg cells developed normally, populated the peripheral lymphoid organs and effectively supressed conventional T cells in vitro. Our data suggest that VPS34 is required for the maturation of Treg cells or that mature Treg cells depend on VPS34 for survival. Functionally, we observed that lack of VPS34 activity impairs cargo processing upon transendocytosis, that defective autophagy contributes to, but is not sufficient to explain this lethal phenotype, and that loss of VPS34 activity induces a state of heightened metabolic activity that may interfere with metabolic networks required for maintenance or suppressive functions of Treg cells.

2024-01-29 | PXD048981 | Pride

TMT characterisation: iPSC vs hESC

Project description:Detailed comparison of human pluripotent stem cells, to determine how hESC and iPSC differ in their protein expression profiles. The data was acquired in a TMT 10-plex SPS-MS3. 4 replicates of hESC compared to 4 replicates of HipSci human iPSCs.

2021-11-03 | PXD014502 | Pride

HipSci: the iPSC proteomic compendium

Project description:Human induced pluripotent stem cell (iPSC) technology holds great potential for therapeutic and research purposes, by providing improved models of disease and for studying mechanisms regulating differentiation. The Human Induced Pluripotent Stem Cell Initiative (HipSci) was established to generate large panel of high-quality human iPSC lines from both healthy donors and disease cohorts for the research community. Here we present a resource featuring a comprehensive proteomic analysis of >200 human iPSC lines obtained from >100 different donors. This dataset has identified in total >16,000 proteins expressed in iPSCs, with expression levels spanning 7 orders of magnitude. Our analysis of these lines has provided insight into mechanisms regulating primed pluripotency. All the proteomics data we have integrated into the Enclyclopedia of Proteome Dynamics where it can be browsed and analysed interactively. https://peptracker.com/epd/analytics

2019-07-25 | PXD010557 | Pride

Proteome of naive and TCR activated wild-type, Myc-deficient and Slc7a5-deficient T cells

Project description:T cell clonal expansion and differentiation are critically dependent on the transcription factor c-Myc (Myc). Herein we use quantitative mass-spectrometry to reveal how Myc controls antigen receptor driven cell growth and proteome restructuring in CD4+ and CD8+ T cells. Quantitative proteomics was performed on naive wild-type (WT) and 24 hr T cell receptor (TCR) activated Myc WT and Myc-deficient T cells. Analysis of copy numbers per cell of >7000 proteins provides new understanding of the selective role of Myc in controlling the protein machinery that shapes T cell fate. The data identify both Myc dependent and independent metabolic processes in immune activated T cells. We uncover that a primary function of Myc is to induce amino acid transporter expression. Quantitative proteomics of 24 hr TCR activated Slc7a5 WT and Slc7a5-deficient CD4 T cells reveals that loss of a single Myc-controlled amino transporter, Slc7a5, can effectively phenocopy the impact of Myc deletion. This study thus provides a comprehensive map of how Myc selectively shapes T cell phenotypes and reveals that Myc induction of amino acid transport is pivotal for subsequent bioenergetic and biosynthetic programs.

2020-02-25 | PXD016105 | Pride

Expression Analysis of Trimethyltin Chlorides (TMT) Impact on Embryonic Development

Project description:Investigation of whole genome expression pattern of 60 and 72 hours post fertilization Danio Rerio embryos exposed to TMT and vehicle control Embryos were exposed to 10uM TMT or control from 48hpf to 60 or 72 hpf. Three replicates were collected for each time point. 40 embryos were pooled to comprise a replicate.

2011-03-23 | E-GEOD-28131 | biostudies-arrayexpress

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