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Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

ABSTRACT: Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

PROVIDER: PRJNA1170949 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30924102.fastq.gz	Fastqsanger.gz
	SRR30924103.fastq.gz	Fastqsanger.gz
	SRR30924104.fastq.gz	Fastqsanger.gz
	SRR30924105.fastq.gz	Fastqsanger.gz

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Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

Project description:Favoring the engraftment and maturation of the engineered HSPCs in the central nervous system could allow enhancing further the therapeutic potential of the transplantation of engineered HSPCs for treating neurometabolic diseases. We propose a gene addition strategy involving Cx3cr1, a microglia chemokine receptor regulating microglia ontogeny and function. Here we characterize the transcriptional profile of microglia-like cell generated by Cx3cr1 haplo-insufficient and WT HSPC

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:CX3CR1, one of the highest expressed genes in microglia in mice and humans, is implicated in numerous microglial functions. However, the molecular mechanisms underlying Cx3cr1 signaling are not well understood. Here, we analyzed transcriptomes of Cx3cr1-deficient microglia under varying conditions by RNA-Seq. In 2 mos mice, Cx3cr1 deletion resulted in the downregulation of a subset of immune-related genes, without substantial epigenetic changes in markers of active chromatin. Surprisingly, Cx3cr1-deficient microglia from young mice exhibited a transcriptome consistent with that of aged Cx3cr1-sufficient animals, suggesting a premature aging transcriptomic signature. Immunohistochemical analysis of microglia in young and aged mice revealed that loss of Cx3cr1 modulates microglial morphology in a compatible fashion. Our results suggest that CX3CR1 may regulate microglial function in part by modulating the expression levels of a subset of inflammatory genes during chronological aging, making Cx3cr1-deficient mice useful for studying aged microglia.

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:Cx3cr1-deficient microglia exhibit a premature aging transcriptome

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:Cx3cr1-deficient microglia exhibit a premature aging transcriptome

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Project description:Memory T cells are important for protective immunity against infectious microorganisms. Such protection is achieved by cooperative action of memory T cell populations that differ in their tissue localization and functionality. We report on the identification of the fractalkine receptor CX3CR1 as marker for stratification of memory T cells with cytotoxic effector function from those with proliferative function in both, mice and man. Based on CX3CR1 and CD62L expression levels four distinct memory T cell populations can be distinguished based on their functional properties. Transcriptome and proteome profiling revealed that CX3CR1 expression was superior to CD62L to resolve memory T cell functionality and allowed determination of a core signature of memory T cells with cytotoxic effector function. This identifies a CD62Lhi CX3CR1+ memory T cell population with an identical gene signature to CD62LlowCX3CR1+ effector memory T cells. In lymph nodes, this so far unrecognized CD62LhiCX3CR1+ T cell population shows a distinct migration pattern and anatomic positioning compared to CD62LhiCX3CR1neg TCM. Furthermore, CX3CR1+ memory T cells were scarce or absent during chronic HBV, HCV and HIV infection in man and chronic LCMV infection in mice confirming the value of CX3CR1+ in understanding principles of protective immune memory. CD8+ T cells were isolated and directly assessed or incubated with DC or LSEC. After harvesting, cells were immediately lysed in Trizol (Invitrogen) before storage at -80Â°C for RNA isolation.

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