Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis. [CD4 - bulk RNAseq]

ABSTRACT: Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis. [CD4 - bulk RNAseq]

PROVIDER: PRJNA665473 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis. [CD4 & CD8 single-cell RNAseq]

Project description:Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis. [CD4 & CD8 single-cell RNAseq]

| PRJNA665472 | ENA

Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis [HSPCs single-cell RNAseq]

Project description:Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis [HSPCs single-cell RNAseq]

| PRJNA665467 | ENA

Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis. [CD4 - bulk RNAseq]

Project description:Whereas the human fetal immune system is poised to generate immune tolerance and suppress inflammation in utero, an adult-like immune system emerges to orchestrate anti-pathogen immune responses in post-natal life. It has been posited that cells of the adult immune system arise as a discrete ontological “layer” of hematopoietic stem-progenitor cells (HSPCs) and their progeny; evidence supporting this model in humans has, however, been inconclusive. Here, we combine bulk and single-cell transcriptional profiling of lymphoid, myeloid, and HSPCs from fetal, perinatal, and adult developmental stages to demonstrate that the fetal-to-adult transition occurs progressively along a continuum of maturity—with a substantial degree of interindividual variation at the time of birth—rather than via a transition between discrete waves. These findings have important implications in the design of strategies for prophylaxis against infection in the newborn, and for the use of umbilical cord blood (UCB) in the setting of transplantation. Naïve CD4 and CD8 T cells, and CD34+ hematopoietic stem and progenitor cells (HSPCs) were isolated from human samples of three different groups: Fetal (18-23 gestational weeks), full-term newborn (37+ gestational weeks at birth), and adults age 23 to 53. For each group, five independent donors were analyzed, but not all cell types could be sequenced for every patient.

2020-09-25 | GSE158491 | GEO

Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis. [CD4 & CD8 single-cell RNAseq]

2020-09-25 | GSE158492 | GEO

Single-cell mapping of progressive fetal-to-adult transition in human hematopoiesis [HSPCs single-cell RNAseq]

2020-09-25 | GSE158490 | GEO

Single-cell mapping of progressive fetal-to-adult transition in human naïve T cells

Project description:Single-cell mapping of progressive fetal-to-adult transition in human naïve T cells

| PRJNA665464 | ENA

Hematopoiesis in Murine Fancd2-/- vs WT Fetal Liver

Project description:Hematopoiesis in Murine Fancd2-/- vs WT Fetal Liver

| PRJNA727546 | ENA

Microglia require CD4 T cells to complete the fetal to adult transition

Project description:Microglia require CD4 T cells to complete the fetal to adult transition

| PRJNA602602 | ENA

Microglia require CD4 T cells to complete the fetal to adult transition

Project description:Microglia require CD4 T cells to complete the fetal to adult transition

| PRJNA609642 | ENA

Sustained fetal hematopoiesis causes juvenile death from leukemia: evidence from a dual-age-specific mouse model

Project description:It is not clear whether disrupted age-specific hematopoiesis contributes to the complex manifestations in leukemia patients who carry identical mutations, particularly in pediatric and adult patients with similar clinical characteristics. By studying a dual-age-specific mouse model, we demonstrate: 1) loss of Pten during the fetal-to-adult hematopoiesis switch (HSC switch) causes sustained fetal hematopoiesis, resulting in death in juvenile leukemia; 2) myeloid-biased hematopoiesis in juvenile mice is associated with the sustained fetal properties of hematopoietic stem cells (HSCs); 3) the age specificity of juvenile myelomonocytic leukemia (JMML) depends on the dosage of Pten and Nf1; 4) single-allelic Pten deletion during the HSC switch causes constitutive activation of mitogen-activated protein kinase (MAPK) in juvenile mice with Nf1 loss of heterozygosity (LOH); and 5) Nf1 LOH causes monocytosis in juvenile mice with Pten haploinsufficiency but does not cause lethality until adulthood. Our data suggest that one copy of Pten is sufficient to maintain an intact negative feedback loop of the Akt pathway and HSC function in reconstitution, despite MAPK being constitutively activated in juvenile mice with Pten+/DNf1LOH. However, two copies of Pten are required to maintain the integrity of the MAPK pathway in juvenile mice with Nf1 haploinsufficiency. Our data indicate that previous investigations of Pten function in wild type mice may not reflect the impact of Pten loss in mice with Nf1 mutations or other genetic defects. We provide a proof-of-concept that disassociated age-specific hematopoiesis contributes to leukemogenesis and pediatric demise.

2020-06-25 | GSE137152 | GEO

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