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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE145230 | GEO | 2020/06/29

REPOSITORIES: GEO

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

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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 (scRNA-seq)

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

Project description:This SuperSeries is composed of the SubSeries listed below.

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Modulation of T cell responses by type I interferons

Project description:Type I interferons (IFNs) play a key role in linking the innate and adaptive immune responses. IFNs can have both positive and negative effects on the development of memory CD8+ T cells, but their contribution to the priming of naÃ¯ve T cells is unclear. Using OT-I TCR transgenic T cells, we show strong effects on TCR-induced functional response when sensitized by IFN-Î² prior to their stimulation with cognate antigen. These effects are only seen in the absence of co-stimulation and at suboptimal TCR stimulation conditions. Pre-stimulation of naÃ¯ve T cells inhibits certain TCR-mediated functions like cell proliferation and the induction of genes such as IFN-Î³ and IL-2. However, type I IFN does not influence the induction of other TCR-induced functions like the expression of the T cell activation marker CD25 and a number of other genes. IFN-mediated impairment of proliferation is due to the lack of IL-2 induction since it can be compensated by exogenous IL-2. Further analysis reveals an IFN-mediated inhibition of Ca2+ flux and ERK phosphorylation. In vivo studies confirm that pre-stimulation with IFNs inhibits early T cell responses, whereas long-term responses are positively affected. Our results reveal that IFN exerts negative effects on naÃ¯ve T cells in a timely defined range under sub-optimal TCR stimulation conditions. These results highlight the importance of timing of immune-regulatory events and reveal a novel role for type I IFNs by shaping the immune response, such that T cells are not able to react until optimal stimulation is provided. 8 Arrays, untreated cells as references, IFNb treatment and/or TCR stimulation at various lengths of time

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