Gene regulatory basis of bystander activation in CD8+ T cells (RNA-seq)
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ABSTRACT:
PROVIDER: PRJNA749293 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15228824.fastq.gz | Fastqsanger.gz | |||
| SRR15228825.fastq.gz | Fastqsanger.gz | |||
| SRR15228826.fastq.gz | Fastqsanger.gz | |||
| SRR15228827.fastq.gz | Fastqsanger.gz | |||
| SRR15228828.fastq.gz | Fastqsanger.gz |
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Project description:Gene regulatory basis of bystander activation in CD8+ T cells
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Project description:Gene regulatory basis of bystander activation in CD8+ T cells (scATAC-seq)
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Project description:Gene regulatory basis of bystander activation in CD8+ T cells (human scRNA-seq)
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Project description:CD8 T cells play a central role in antiviral immunity. Type I interferons are among the earliest responders after virus exposure and can cause extensive reprogramming and antigen-independent bystander activation of CD8 T cells. Although bystander activation of pre-existing memory CD8 T cells is known to play an important role in host defense and immunopathology, its impact on naïve CD8 T cells remains underappreciated. Here we report that exposure to reovirus, both in vitro or in vivo, promotes bystander activation of naïve CD8 T cells within 24 hours and that this distinct subtype of CD8 T cell displays an innate, antiviral, type I interferon sensitized signature. The induction of bystander naïve CD8 T cells is STAT1 dependent and regulated through nicotinamide phosphoribosyl transferase (NAMPT)-mediated enzymatic actions within NAD+ salvage metabolic biosynthesis. These findings identify a novel aspect of CD8 T cell activation following virus infection with implications for human health and physiology.
2023-01-30 | PXD039614 | Pride
Project description:CD8+ T cells have been categorized as an adaptive lymphocyte, based on their ability to recognize specific foreign antigens and mount memory responses. However, neonatal and adult CD8+ T cells are derived from distinct HSC progenitors, which may alter the roles they play during infection. Here, we demonstrate that neonatal CD8+ T cells can be activated by innate cytokines alone and protect the host from a variety of unrelated pathogens in the absence of TCR signaling. Using a multi-omics approach, we found that neonatal CD8+ T cells are highly responsive to innate cytokines because they can rapidly undergo chromatin remodeling, resulting in the usage of a distinct set of enhancers that are more commonly found in innate-like T cells. We also identified a key gene regulatory axis (Bach2/AP1) that is differentially utilized by neonatal and adult CD8+ T cells to toggle their responsiveness to innate cytokines. Importantly, the developmental switch between innate and adaptive functions in the CD8+ T cell compartment is not mediated by a change in the maturation of individual cells along a linear axis, but rather by changes in the abundance of distinct subsets of cells. Collectively, our findings provide support for the layered immune hypothesis and indicate that the CD8+ T cell compartment is more phenotypically diverse than previously thought.
2024-02-26 | GSE218223 | GEO
Project description:CD8+ T cells have been categorized as an adaptive lymphocyte, based on their ability to recognize specific foreign antigens and mount memory responses. However, neonatal and adult CD8+ T cells are derived from distinct HSC progenitors, which may alter the roles they play during infection. Here, we demonstrate that neonatal CD8+ T cells can be activated by innate cytokines alone and protect the host from a variety of unrelated pathogens in the absence of TCR signaling. Using a multi-omics approach, we found that neonatal CD8+ T cells are highly responsive to innate cytokines because they can rapidly undergo chromatin remodeling, resulting in the usage of a distinct set of enhancers that are more commonly found in innate-like T cells. We also identified a key gene regulatory axis (Bach2/AP1) that is differentially utilized by neonatal and adult CD8+ T cells to toggle their responsiveness to innate cytokines. Importantly, the developmental switch between innate and adaptive functions in the CD8+ T cell compartment is not mediated by a change in the maturation of individual cells along a linear axis, but rather by changes in the abundance of distinct subsets of cells. Collectively, our findings provide support for the layered immune hypothesis and indicate that the CD8+ T cell compartment is more phenotypically diverse than previously thought.
2024-02-26 | GSE218456 | GEO
Project description:CD8+ T cells have been categorized as an adaptive lymphocyte, based on their ability to recognize specific foreign antigens and mount memory responses. However, neonatal and adult CD8+ T cells are derived from distinct HSC progenitors, which may alter the roles they play during infection. Here, we demonstrate that neonatal CD8+ T cells can be activated by innate cytokines alone and protect the host from a variety of unrelated pathogens in the absence of TCR signaling. Using a multi-omics approach, we found that neonatal CD8+ T cells are highly responsive to innate cytokines because they can rapidly undergo chromatin remodeling, resulting in the usage of a distinct set of enhancers that are more commonly found in innate-like T cells. We also identified a key gene regulatory axis (Bach2/AP1) that is differentially utilized by neonatal and adult CD8+ T cells to toggle their responsiveness to innate cytokines. Importantly, the developmental switch between innate and adaptive functions in the CD8+ T cell compartment is not mediated by a change in the maturation of individual cells along a linear axis, but rather by changes in the abundance of distinct subsets of cells. Collectively, our findings provide support for the layered immune hypothesis and indicate that the CD8+ T cell compartment is more phenotypically diverse than previously thought.
2024-03-11 | GSE261140 | GEO
Project description:Background: Memory CD8+ T cells sense inflammation and rapidly produce interferon-γ (IFN-γ) independent of cognate antigens. This innate-like property, called bystander activation, is involved in early host defense before the antigen-specific memory response. However, the molecular mechanisms underlying this activation remain unknown. Retinoic acid receptor-related orphan receptor α (RORα) belongs to the nuclear receptor family and regulates gene transcription in ligand-dependent manner. Although RORα is highly expressed in memory CD8+ T cells, its functional relevance has not been investigated. Methods: Primary and secondary memory T cells that are sufficient or deficient of RORα were induced by adoptive transfer of naïve OT-I T cells to recipient mice and subsequent infection with Listeria monocytogenes expressing ovalbumin (LM-OVA). RORα expression in memory T cells were examined by quantitative PCR. The target genes of RORα in memory T cells were explored by RNA-sequencing and verified by RORα overexpression in postactivated T cells. The impact of RORα-deficiency on bystander activation was assessed by stimulating memory T cells with inflammatory cytokines in vitro or injecting lipopolysaccharide (LPS) into mice bearing memory T cells. Results: RORα expression was remarkably elevated in secondary memory CD8+ T cells along with the enrichment of effector-like memory T cells. RORα primarily acted as a transcription factor in regulating the gene expression of the TL1A receptor. RORα deficiency abrogated the IFN-γ production by memory CD8+ T cells in response to IL-12 + TL1A in vitro and diminished the bystander response to LPS-induced inflammation in vivo. Conclusion: This study revealed a regulatory mechanism of bystander activation. The findings also improve our understanding of how memory T cells increase their immediate protective capacity through repeated infections and vaccinations.
2025-08-03 | GSE304290 | GEO