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Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism

ABSTRACT: Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism

PROVIDER: PRJNA606470 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR11077449.fastq.gz	Fastqsanger.gz
	SRR11077450.fastq.gz	Fastqsanger.gz
	SRR11077451.fastq.gz	Fastqsanger.gz
	SRR11077452.fastq.gz	Fastqsanger.gz

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Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism (scRNA-seq)

Project description:Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism (scRNA-seq)

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Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism (bulkRNA-seq)

Project description:Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism (bulkRNA-seq)

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Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism (scRNA-seq)

Project description:Differences in female and male immunity may contribute to variations in response to infections and predisposition to autoimmunity. The characterization of the mechanisms that drive differential neutrophil phenotypes between genders has been investigated. This provides new insights that distinct sex difference in neutrophil biology related to responses to type I IFNs, immunometabolism and maturation status that may have prominent functional and pathogenic implications. The transcriptome of neutrophils from healthy adult males and females was characterized using bulk RNASeq. The transcriptome of whole blood leukocytes was elucidated using scRNASeq.

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Sex differences in neutrophil biology modulate response to type I interferons and immunometabolism.

Project description:Differences between female and male immunity may contribute to variations in response to infections and predisposition to autoimmunity. We previously reported that neutrophils from reproductive-age males are more immature and less activated than their female counterparts. To further characterize the mechanisms that drive differential neutrophil phenotypes, we performed RNA sequencing on circulating neutrophils from healthy adult females and males. Female neutrophils displayed significant up-regulation of type I IFN (IFN)-stimulated genes (ISGs). Single-cell RNA-sequencing analysis indicated that these differences are neutrophil specific, driven by a distinct neutrophil subset and related to maturation status. Neutrophil hyperresponsiveness to type I IFNs promoted enhanced responses to Toll-like receptor agonists. Neutrophils from young adult males had significantly increased mitochondrial metabolism compared to those from females and this was modulated by estradiol. Assessment of ISGs and neutrophil maturation genes in Klinefelter syndrome (47, XXY) males and in prepubescent children supported that differences in neutrophil phenotype between adult male and female neutrophils are hormonally driven and not explained by X chromosome gene dosage. Our results indicate that there are distinct sex differences in neutrophil biology related to responses to type I IFNs, immunometabolism, and maturation status that may have prominent functional and pathogenic implications.

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Sex differences in neutrophil biology modulate response to type I Interferons and immunometabolism

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The effect of interferons on presentation of defective ribosome products as HLA peptides

Project description:The class I major histocompatibility complex (MHC) bound peptides, produced from immature proteins that are degraded rapidly are called defective ribosome products (DRiPs). Such DRiPs are possibly involved with early alerting of the immune system about impeding infections, thus bringing about faster killing of infected cells before the viruses replicate. Interferons are a major group of cytokines, produced in response to viral infection. The interferons modulate the cellular metabolism and gene expression patterns and increase the expression and cell-surface presentation of the MHC molecules, helping this way coping with the viral infection. In this study, we evaluated whether the interferons also induce rapid degradation of cellular or viral proteins and produce DRiPs MHC-bound peptides to help the alert of the immune system. Cultured human breast cancer cells were treated with interferons and the cells were transferred to growth media containing heavy stable isotope labeled amino acids (dynamic-SILAC)in several time points a few hours after the interferons’ treatment. The rates of synthesis, degradation, and production of the cellular protein and their degradation products, the MHC peptides, were followed by LC-MS/MS analyses. Detection of large numbers of MHC peptides that incorporate the heavy amino acids into them, faster than their source proteins, indicated to us that not only DRiP-peptides are rather abundant among the MHC peptidome, but that the interferons increase significantly the presentation of DRiP-peptides. Importantly, much of this DRiPome derive from multi-subunit complexes, including the proteasomes and ribosomes, while the degradation of the standard protostome give rise to the immunoproteasome, which is thought to produce peptides that enhance the immune-response; the degradation of the ribosome subunits may aid in reducing the synthesis of viral infection

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