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Innate immune cell memory induced by endogenous and exogenous triggers

ABSTRACT: innate immune cell memory induced by endogenous and exogenous triggers

PROVIDER: PRJNA1143447 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR30113403_1.fastq.gz	Fastqsanger.gz
	SRR30113403_2.fastq.gz	Fastqsanger.gz
	SRR30113404_1.fastq.gz	Fastqsanger.gz
	SRR30113404_2.fastq.gz	Fastqsanger.gz

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innate immune cell memory induced by endogenous and exogenous triggers

Project description:Innate memory is a key defence mechanism against infection, enhancing protective immunity and limiting unnecessary collateral tissue damage. Inflammation triggered by endogenous stimuli that signal cellular stress or tissue injury, must also be tightly controlled to balance robust response to intrinsic danger whilst avoiding catastrophic autoimmunity. Here, we assess the contribution of innate memory to this balance. The extracellular matrix protein tenascin-C, a damage-associated, toll-like receptor 4 (TLR4) agonist, reprograms monocyte response to subsequent threat, inducing concomitantly suppressed and enhanced responses to rechallenge. Comparative analysis of memory evoked by tenascin-C and the pathogenic TLR4 agonist, LPS, revealed both common and distinct gene expression signatures, effects that were controlled transcriptionally, These data highlight how intrinsic and extrinsic innate re-programming exerts control over dysregulated inflammatory networks driving either infectious or chronic ‘sterile’ inflammatory diseases.

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ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (expression)

Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe expression profile of peritoneal macrophages from wild-type mice pre-administrated with TLR ligands or from ATF7 knockout mice. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory. This series contains seven sets of exression array data. For all sample, we use four CEL files generated by four biological-independent experiments.

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Project description:Memory CD8+ T cells have the ability to provide lifelong immunity against pathogens. Although memory features generally arise after challenge with a foreign antigen, naïve CD8 single positive (SP) thymocytes may acquire phenotypic and functional characteristics of memory cells in response to cytokines such as interleukin-4. This process is associated with the induction of the T-box transcription factor Eomesodermin (EOMES). However, the underlying molecular mechanisms remain ill-defined. Using epigenomic profiling, we show that these innate memory CD8SP cells acquire only a portion of the active enhancer repertoire of conventional memory cells. This reprograming is secondary to EOMES recruitment, mostly to RUNX3-bound enhancers. Furthermore, EOMES is found within chromatin-associated complexes containing BRG1 and promotes the recruitment of this chromatin remodelling factor. Also, the in vivo acquisition of EOMES-dependent program is BRG1-dependent. In conclusion, our results support a strong epigenetic basis for the EOMES-driven establishment of CD8+ T cell innate memory program.

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