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Mitochondrial respiration contributes to the interferon gamma response in antigen presenting cells

ABSTRACT: Mitochondrial respiration contributes to the interferon gamma response in antigen presenting cells

PROVIDER: PRJNA681904 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13177435.fastq.gz	Fastqsanger.gz
	SRR13177436.fastq.gz	Fastqsanger.gz
	SRR13177437.fastq.gz	Fastqsanger.gz
	SRR13177438.fastq.gz	Fastqsanger.gz
	SRR13177439.fastq.gz	Fastqsanger.gz

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Mitochondrial respiration contributes to the interferon gamma response in antigen presenting cells

Project description:Antigen presenting cells (APC) act as an integration point where signaling and metabolic pathways collaboratively determine cellular activation state and shape T cell responses. We performed a series of genome-wide knockout screens in interferon gamma (IFNg)-stimulated macrophages, identifying overlapping sets of regulators that control the expression of the T cell stimulatory or inhibitory proteins, MHCII, CD40, and PD-L1. This multi-screen approach defined novel pathways that differentially control these functionally-distinct proteins, and identified mitochondrial function as a global regulator of the IFNg response. Specifically, we report that complex I of the mitochondrial respiratory chain is necessary for signal transduction via the IFNgreceptor, and consequently for both macrophages and dendritic cells to function as APCs. The importance of mitochondrial function for the IFNg response contrasts with the known glycolytic dependency of pattern-recognition receptor stimulation, implicating metabolic state as a fulcrum of innate immunity.

2021-11-01 | GSE162463 | GEO

Mitochondrial respiration contributes to the interferon gamma response in antigen-presenting cells.

Project description:The immunological synapse allows antigen-presenting cells (APCs) to convey a wide array of functionally distinct signals to T cells, which ultimately shape the immune response. The relative effect of stimulatory and inhibitory signals is influenced by the activation state of the APC, which is determined by an interplay between signal transduction and metabolic pathways. While pathways downstream of toll-like receptors rely on glycolytic metabolism for the proper expression of inflammatory mediators, little is known about the metabolic dependencies of other critical signals such as interferon gamma (IFNγ). Using CRISPR-Cas9, we performed a series of genome-wide knockout screens in murine macrophages to identify the regulators of IFNγ-inducible T cell stimulatory or inhibitory proteins MHCII, CD40, and PD-L1. Our multiscreen approach enabled us to identify novel pathways that preferentially control functionally distinct proteins. Further integration of these screening data implicated complex I of the mitochondrial respiratory chain in the expression of all three markers, and by extension the IFNγ signaling pathway. We report that the IFNγ response requires mitochondrial respiration, and APCs are unable to activate T cells upon genetic or chemical inhibition of complex I. These findings suggest a dichotomous metabolic dependency between IFNγ and toll-like receptor signaling, implicating mitochondrial function as a fulcrum of innate immunity.

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Interferon dependent genes of intrathymic antigen presenting cells

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Project description:Assessing the gene expression repertoire of antigen presenting dendritic cells Keywords: other

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Project description:Transcriptional profiles of four different myeloid antigen presenting cell (APC) subsets (BDCA-1+ circulating myeloid dendritic cells, CD14+ monocytes, and in vitro generated immature and mature monocyte-derived dendritic cells) were used for comprehensive transcriptome analysis. Based on the gene expression profiling data, a quantitative relationship between myeloid APC in functionally related gene spaces was established. Keywords = myeloid antigen presenting cells Keywords = dendritic cell subsets Keywords: repeat sample

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Project description:Dr. van Kooyk's laboratory is exploring the function of antigen presenting cells, such as dendritic cells (DC), that regulate viral-antigen recognition, DC trafficking and T cell binding--all processes that initiate immunity or tolerance. Essential in this is the recognition of ligands by C-type lectins and the functional consequences of differential terminal glycosylation that may regulate DC function. In this study, the gene expression profile of glycosylation-related genes is examined in relation to the maturation of human antigen-presenting cells. Two pooled RNA samples, one each from immature and mature human monocyte-derived dendritic cells, were prepared and sent to Microarray Core (E). The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays.

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