CD62L expression level determines the cell fate of myeloid progenitors in mice and humans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA699169 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13618261_1.fastq.gz | Fastqsanger.gz | |||
| SRR13618261_2.fastq.gz | Fastqsanger.gz | |||
| SRR13618262_1.fastq.gz | Fastqsanger.gz | |||
| SRR13618262_2.fastq.gz | Fastqsanger.gz | |||
| SRR13618263_1.fastq.gz | Fastqsanger.gz |
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Project description:Through gene expression analysis of CMPs and GMPs at single cell levels, we identified CD62L as a marker to reveal the heterogeneity of CMPs and GMPs. We confirmed that the CD62L-low CMPs represent ‘bona fide’ CMPs, whereas CD62L-high CMPs are mostly restricted to GMP potentials both in mice and humans. In addition, we identified CD62L-neg GMPs as the most immature subsets in GMPs and Ly6c+CD62L-low and Ly6c+CD62L-high GMPs are skewed to neutrophil and monocyte differentiation, respectively. We performed gene expression profiling of CD62L-low CMPs, CD62L-high CMPs, CD62L-neg GMPs, CD62L-low GMPs, CD62L-high GMPs, bulk CMPs, and bulk GMPs.
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Project description:Hematopoietic cells differentiate through several progenitors in a hierarchical manner, and recent single-cell analyses have revealed substantial heterogeneity within each progenitor. Although common myeloid progenitors (CMPs) are defined as a multipotent cell population that can differentiate into granulocyte-monocyte progenitors (GMPs) and megakaryocyte-erythrocyte progenitors (MEPs), and GMPs generate neutrophils and monocytes, these myeloid progenitors must contain some lineage-committed progenitors. Through gene expression analysis at single-cell levels, we identified CD62L as a marker to reveal the heterogeneity. We confirmed that CD62L-negative CMPs represent "bona fide" CMPs, whereas CD62L-high CMPs are mostly restricted to GMP potentials both in mice and humans. In addition, we identified CD62L-negative GMPs as the most immature subsets in GMPs and Ly6C+CD62L-intermediate and Ly6C+CD62L-high GMPs are skewed to neutrophil and monocyte differentiation in mice, respectively. Our findings contribute to more profound understanding about the mechanism of myeloid differentiation.
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Project description:The memory B cell response consists of phenotypically distinct subsets that differ in their ability to respond upon antigen re-encounter. However, the pathways regulating the development and function of memory B cell subsets are poorly understood. Here we show that CD62L and CD44 are progressively expressed on mouse memory B cells and identify transcriptionally and functionally distinct memory B cell subsets. Bcl6 is important in regulating memory B cell subset differentiation with overexpression of Bcl6 resulting in impaired CD62L+ memory B cell development. Bcl6 regulates memory B cell subset development through control of a network of genes, including Bcl2 and Zeb2. Overexpression of Zeb2 impairs the development of CD62L+ memory B cells. Importantly, CD62L is also differentially expressed on human memory B cells following SARS-CoV-2 vaccination and identifies phenotypically distinct populations. Together, these data indicate that CD62L expression marks functionally distinct memory B cell subsets.
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Project description:A network of co-hepato/pancreatic stem/progenitors exists in pigs and humans in Brunner’s Glands (BGs) in the submucosa of the duodenum, in peribiliary glands (PBGs) of intrahepatic and extrahepatic biliary trees, and in pancreatic duct glands (PDGs) of intrapancreatic biliary trees, collectively supporting hepatic and pancreatic regeneration postnatally. The network is found in humans postnatally throughout life and, so far, has been demonstrated in pigs postnatally at least through to young adults. These stem/progenitors in vivo in pigs are in highest numbers in BGs and in PDGS nearest the duodenum, and in humans are in BGs and in PBGs in the hepato/pancreatic common duct, a duct missing postnatally in pigs. Elsewhere in PDGs in pigs and in all PDGs in humans are only committed unipotent or bipotent progenitors.
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Project description:Ortega2013 - Interplay between secretases
determines biphasic amyloid-beta level
This model is described in the article:
Interplay between ?-, ?-,
and ?-secretases determines biphasic amyloid-? protein level in
the presence of a ?-secretase inhibitor.
Ortega F, Stott J, Visser SA,
Bendtsen C.
J. Biol. Chem. 2013 Jan; 288(2):
785-792
Abstract:
Amyloid-? (A?) is produced by the consecutive cleavage of
amyloid precursor protein (APP) first by ?-secretase,
generating C99, and then by ?-secretase. APP is also cleaved by
?-secretase. It is hypothesized that reducing the production of
A? in the brain may slow the progression of Alzheimer disease.
Therefore, different ?-secretase inhibitors have been developed
to reduce A? production. Paradoxically, it has been shown that
low to moderate inhibitor concentrations cause a rise in A?
production in different cell lines, in different animal models,
and also in humans. A mechanistic understanding of the A? rise
remains elusive. Here, a minimal mathematical model has been
developed that quantitatively describes the A? dynamics in cell
lines that exhibit the rise as well as in cell lines that do
not. The model includes steps of APP processing through both
the so-called amyloidogenic pathway and the so-called
non-amyloidogenic pathway. It is shown that the cross-talk
between these two pathways accounts for the increase in A?
production in response to inhibitor, i.e. an increase in C99
will inhibit the non-amyloidogenic pathway, redirecting APP to
be cleaved by ?-secretase, leading to an additional increase in
C99 that overcomes the loss in ?-secretase activity. With a
minor extension, the model also describes plasma A? profiles
observed in humans upon dosing with a ?-secretase inhibitor. In
conclusion, this mechanistic model rationalizes a series of
experimental results that spans from in vitro to in vivo and to
humans. This has important implications for the development of
drugs targeting A? production in Alzheimer disease.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000556.
To cite BioModels Database, please use:
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quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
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Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000556 | BioModels
Project description:Two subsets of stem-like CD8+ memory T cell progenitors with distinct fate commitments in humans
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Project description:Two subsets of stem-like CD8+ memory T cell progenitors with distinct fate commitments in humans
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Project description:Human Natural Killer (NK) cells comprise two main subsets, CD56bright and CD56dim cells, that differ in function, phenotype and tissue localization. To further dissect the heterogeneity of CD56dim cells, we have performed transcriptome analysis and functional ex vivo characterization of human NK cell subsets according to the expression of markers related to differentiation, migration or competence. Here, we show for the first time that the ability to respond to cytokines or to activating receptors is mutually exclusive in almost all NK cells with the exception of CD56dim CD62L+ cells. Indeed, only these cells combine the ability to produce interferon (IFN)-gamma after cytokines and proliferate in vivo during viral infection with the capacity to kill and produce cytokines upon engagement of activating receptors. Therefore, CD56dim CD62L+ cells represent a unique subset of polyfunctional NK cells. Ex vivo analysis of their function, phenotype, telomere length, frequencies during ageing as well as transfer experiments of NK cell subsets into immunodeficient mice suggest that CD56dim CD62L+ cells represent an intermediate stage of NK cell maturation, which after restimulation can accomplish multiple tasks and further develop into terminally differentiated effectors. Gene expression profiles of FACSAria sorted CD3- CD56bright CD62L+, CD3- CD56dim CD62L+ and CD3- CD56dim CD62L- NK cells from human peripheral blood of three donors were compared using Affymetrix GeneChip Human Genome HG-U133_Plus_2. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 µg cRNA hybridized in triplicates for each of the three groups to the GeneChip arrays. Group1: CD3- CD56bright CD62L+,.Group2: CD3- CD56dim CD62L+, Group3: CD3- CD56dim CD62L-. Lists of differentially regulated genes were created using High Performance Chip Data Analysis (HPCDA) with Bioretis database (http://www.bioretis-analysis.de). Worldwide data sharing is possible via Bioretis, please ask the authors.
2010-05-28 | E-GEOD-21774 | biostudies-arrayexpress