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

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

PROVIDER: PRJNA609642 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11213591.fastq.gz	Fastqsanger.gz
	SRR11213592.fastq.gz	Fastqsanger.gz

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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:The blood brain barrier has long been thought to isolate the brain from the adaptive immune system. While CD4 T cells have been reported in the central nervous system, their presence in the healthy brain remains controversial, and their function at this site unknown. Here we have used a combination of imaging, single cell and surgical approaches to identify a unique CD69+ CD4 T cell population in both the mouse and human brain, which is distinct from circulating CD4 T cells. The brain-resident population was derived through in situ differentiation from activated circulatory cells, and was shaped by interaction with the gut microbiome and self-antigen in the brain. Single cell sequencing revealed that in the absence of murine CD4 T cells, resident microglia remained suspended between a fetal and adult state. This maturation defect resulted in excess immature neuronal synapses and behavioral abnormalities in the adult mouse. These results illuminate a role for CD4 T cells in the basic developmental processes of the brain, and a potential interconnected dynamic between the evolution of the immunological and neurological systems.

2020-07-27 | GSE144038 | GEO

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

2020-07-27 | GSE146165 | GEO

Microglia Require CD4 T Cells to Complete the Fetal-to-Adult Transition.

Project description:The brain is a site of relative immune privilege. Although CD4 T cells have been reported in the central nervous system, their presence in the healthy brain remains controversial, and their function remains largely unknown. We used a combination of imaging, single cell, and surgical approaches to identify a CD69+ CD4 T cell population in both the mouse and human brain, distinct from circulating CD4 T cells. The brain-resident population was derived through in situ differentiation from activated circulatory cells and was shaped by self-antigen and the peripheral microbiome. Single-cell sequencing revealed that in the absence of murine CD4 T cells, resident microglia remained suspended between the fetal and adult states. This maturation defect resulted in excess immature neuronal synapses and behavioral abnormalities. These results illuminate a role for CD4 T cells in brain development and a potential interconnected dynamic between the evolution of the immunological and neurological systems. VIDEO ABSTRACT.

| S-EPMC7427333 | biostudies-literature

Transcriptomic analysis of human fetal microglia during mid-trimester gestation

Project description:Microarray analysis of human fetal microglia from the mid-trimester period was performed. DEGs were identified between early and late stages of the mid-trimester gestation. Genes expressed in the human fetal microglia were also compared with mouse microglia core signature.

2017-11-21 | GSE107128 | GEO

Microglia in developing retina transition through a disease-like functional state that does not require CSF1R signaling for survival

Project description:Microglia have important remodeling functions in development and disease. There is evidence for molecular diversity of microglia suggesting they may exist in distinct functional states to differentially impact CNS health and function. To better understand this in development, we profiled microglia of a discrete developing CNS region, the murine retina. We find that retinal microglia transition through unique transcriptional states and identify a population with peak density postnatally that resemble adult disease-associated microglia (DAM) and CD11c+ microglia of developing white matter, we term DAM-like. Developmental cell death is a major driver of the DAM-like phenotype, and TREM2 signaling is required for select DAM gene expression. Notably, DAM-like cells that highly express CD11c are not dependent on CSF1R signaling for survival, and TREM2 signaling is required for CSF1R independence in a subset of microglia. Thus, microglial phenotype in development is influenced by local developmental events and may share features with microglia in disease.

2019-06-10 | GSE123757 | GEO

Microglia in developing retina transition through a disease-like functional state that does not require CSF1R signaling for survival

Project description:Microglia in developing retina transition through a disease-like functional state that does not require CSF1R signaling for survival

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Fetal brain response to maternal inflammation requires microglia

Project description:Fetal brain response to maternal inflammation requires microglia

| PRJNA935747 | ENA

Single cell transcriptomics and chromatin accessibility in human fetal microglia

Project description:Microglia, the myeloid cells of the central nervous system (CNS), are heterogeneous and exhibit distinct stages during mouse development; however, human microglia development is not elucidated. Here, single cell gene expression profiles of 15,782 human microglia and bulk chromatin profiles were assessed in 23 fetuses during development from gestational week (GW) 9 to 18. Microglia are highly heterogeneous at all developmental stages and exhibit transcriptional profiles similar to a phagocytic microglia phenotype associated with disease. Microglia start to mature during this developmental period and increasingly express homeostatic and sensome markers at later gestational stages. Concomitantly, chromatin accessibility increases in microglia from older fetuses with underlying transcriptional networks reminiscent of adult microglia. In conclusion, this work demonstrates that microglia already progress to a more mature, immune-sensing competent phenotype during early human fetal development, which might render microglia vulnerable towards environmental or inflammatory perturbations during early pregnancy.

2020-07-31 | GSE141862 | GEO

Fetal brain response to maternal inflammation requires microglia [Maternal_Inflammation]

Project description:In utero infection and maternal inflammation can adversely impact fetal brain development. Maternal systemic illness, even in the absence of direct fetal central nervous system infection, is associated with an increased risk of autism and schizophrenia in affected offspring. The cell types mediating the response of the fetal brain to maternal inflammation are largely unknown, hindering the development of therapies to prevent and treat adverse neuropsychiatric outcomes. Here, we show that microglia are enriched for expression of receptors for relevant pathogens and cytokines throughout embryonic development.

2024-05-07 | GSE225430 | GEO

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