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Stress granule assembly impairs macrophage efferocytosis [RNA-seq]

ABSTRACT: Stress granule assembly impairs macrophage efferocytosis [RNA-seq]

PROVIDER: PRJNA1101040 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28709700_1.fastq.gz	Fastqsanger.gz
	SRR28709700_2.fastq.gz	Fastqsanger.gz
	SRR28709701_1.fastq.gz	Fastqsanger.gz
	SRR28709701_2.fastq.gz	Fastqsanger.gz
	SRR28709702_1.fastq.gz	Fastqsanger.gz

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Project description:Stress granules (SGs) assembly in response to various stress, has been demonstrated in the regulation of anti-viral immune response and tumor progression. However, lack of evidence to illustrate the relation between SGs formation and allergic diseases. Applied G3BP1-RIP-seq in RAW264.7 cells, G3BP1 binding mRNAs are defined.

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Study of human macrophage reprogramming toward a pro-resolving profile by efferocytosis

Project description:Inﬂammation is a physiopathological process triggered by infection or tissue damage. Immune system initiates coordinated sequential steps in response to these danger signals. Once the threat has been contained inflammation has to be subsequently shut down. Inflammation resolution is initiated by the reprogramming of pro-inflammatory macrophages toward a pro-resolving profile. This reprogramming is induced in particular by the non-phlogistic engulfment of apoptotic cells, mostly apoptotic neutrophils, a process called efferocytosis. As a matter of fact, macrophages are an essential linchpin regulating both inflammation triggering and sustaining and inflammation resolution. This duality can be achieved through the tremendous plasticity of these innate immune cells. Indeed, depending on microenvironmental signals (cytokines, efferocytosis, growth factors…) macrophages can adopt numerous diverse and sometimes antagonistic phenotypes. The mechanisms governing these transitions remain relatively scattered especially in human. With this project we propose to explore the mechanisms involved in human macrophage reprogramming toward a pro-resolving profile after efferocytosis. The stakes are high due to the estimated prevalence of chronic inflammatory diseases in Western society is 5 to 7%. Chronic inflammation is a burden to patient due to life-long debilitating illness and increased mortality and is also a burden to society due to high costs for therapy and care. Finding new therapies to limit chronic inflammation establishment and persistence is thus a highly valuable goal.

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