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Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone

ABSTRACT: Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone

PROVIDER: PRJNA564143 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10075964_1.fastq.gz	Fastqsanger.gz
	SRR10075964_2.fastq.gz	Fastqsanger.gz
	SRR10075965_1.fastq.gz	Fastqsanger.gz
	SRR10075965_2.fastq.gz	Fastqsanger.gz
	SRR10075966_1.fastq.gz	Fastqsanger.gz

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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.

2020-01-01 | GSE136972 | GEO

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

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

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

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

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

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Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone

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

2020-01-01 | GSE136980 | GEO

Long-Term Programming of CD8 T Cell Immunity by Perinatal Exposure to Glucocorticoids.

Project description:Early life environmental exposure, particularly during perinatal period, can have a life-long impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptations 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-pituitary-adrenal (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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Prenatal inflammation remodels lung immunity and function by programming ILC2 hyperactivation

Project description:We examined how prenatal inflammation shapes tissue function and immunity in the lung by reprogramming tissue-resident immune cells from early development. Maternal, but not fetal, type I interferon-mediated inflammation provoked expansion and hyperactivation of group 2 innate lymphoid cells (ILC2s) seeding the developing lung. Hyperactivated ILC2s produced increased IL-5 and IL-13, were associated with acute Th2 bias, decreased Tregs, and persistent lung eosinophilia into adulthood. ILC2 hyperactivation was recapitulated by adoptive transfer of a fetal liver precursor following prenatal inflammation, indicative of developmental programming at the fetal progenitor level. Reprogrammed ILC2 hyperactivation and subsequent lung immune remodeling, including persistent eosinophilia, was associated with worsened histopathology and increased airway dysfunction equivalent to papain exposure, indicating increased asthma susceptibility in offspring. Our data elucidate a potential mechanism by which early-life inflammation results in increased asthma susceptibility, driven by hyperactivated ILC2s that drive persistent changes to lung immunity during perinatal development.

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2013-08-01 | E-GEOD-46551 | biostudies-arrayexpress

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