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Early microbial exposure shapes adult immunity by altering CD8+ T cell development

ABSTRACT: Early microbial exposure shapes adult immunity by altering CD8+ T cell development

PROVIDER: PRJNA882501 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21648200_1.fastq.gz	Fastqsanger.gz
	SRR21648200_2.fastq.gz	Fastqsanger.gz
	SRR21650400_1.fastq.gz	Fastqsanger.gz
	SRR21650400_2.fastq.gz	Fastqsanger.gz
	SRR21648201_1.fastq.gz	Fastqsanger.gz

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Early microbial exposure shapes adult immunity by altering CD8+ T cell development [RNA-seq]

Project description:Early microbial exposure shapes adult immunity by altering CD8+ T cell development [RNA-seq]

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Early microbial exposure shapes adult immunity by altering CD8+ T cell development [ATAC-seq]

Project description:Early microbial exposure shapes adult immunity by altering CD8+ T cell development [ATAC-seq]

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Early microbial exposure shapes adult immunity by altering CD8+ T cell development [ATAC-seq]

Project description:Microbial exposure during development can elicit long-lasting effects on the health of an individual. However, how microbial exposure in early life leads to permanent changes in the immune system is unknown. Here, we show that the microbial environment alters the setpoint for immune susceptibility by altering the developmental architecture of the CD8+ T cell compartment. In particular, early microbial exposure results in the preferential expansion of highly responsive fetal-derived CD8+ T cells that persist into adulthood and provide the host with enhanced immune protection against intracellular pathogens. Interestingly, microbial education of fetal-derived CD8+ T cells occurs during thymic development rather than in the periphery and involves the acquisition of a more effector-like epigenetic program. Collectively, our results provide a new conceptual framework for understanding how microbial colonization in early life leads to lifelong, and potentially irreversible, changes in the immune system.

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Early microbial exposure shapes adult immunity by altering CD8+ T cell development [RNA-seq]

2022-12-04 | GSE213829 | GEO

Early microbial exposure shapes adult immunity by altering CD8+ T cell development.

Project description:Microbial exposure during development can elicit long-lasting effects on the health of an individual. However, how microbial exposure in early life leads to permanent changes in the immune system is unknown. Here, we show that the microbial environment alters the set point for immune susceptibility by altering the developmental architecture of the CD8+ T cell compartment. In particular, early microbial exposure results in the preferential expansion of highly responsive fetal-derived CD8+ T cells that persist into adulthood and provide the host with enhanced immune protection against intracellular pathogens. Interestingly, microbial education of fetal-derived CD8+ T cells occurs during thymic development rather than in the periphery and involves the acquisition of a more effector-like epigenetic program. Collectively, our results provide a conceptual framework for understanding how microbial colonization in early life leads to lifelong changes in the immune system.

| S-EPMC9894172 | biostudies-literature

Early microbial exposure shapes adult immunity by altering CD8+ T cell development

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

2022-12-04 | GSE213831 | GEO

Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [ATAC-seq]

Project description:Early life environmental exposure, particularly during perinatal period, can have a lifelong impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptation to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitaryadrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.

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Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [RNA-seq]

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Tenascin-C shapes TRAIL control over tumor immunity

Project description:Tenascin-C shapes TRAIL control over tumor immunity

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Senescent cells display an altered immunopeptidome and promote CD8-dependent antitumor immunity

Project description:Cellular senescence is a stress response known to activate innate immunity. However, how senescent cells interact with the adaptive immune system remains largely unexplored. Here, we show that senescent cells display an enhanced MHC class I antigen processing and presentation. Furthermore, senescent cells present an altered immunopeptidome including unique non-mutated antigens that can be recognized by specific CD8 T cells. Immunization of mice with senescent cancer cells triggers strong protective CD8-dependent antitumor responses, superior to immunogenic cell death. Similarly, induction of senescence in human primary cancer cells hyperactivates their cognate reactive CD8 T cell. Our study indicates that immunization with senescent cells provides a sustained source of antigens that strongly activate anti-tumor CD8 T cells.

2022-10-18 | PXD033714 | Pride

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