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Natural genetic variation reveals key features of epigenetic and transcriptional memory in virus-specific CD8 T cells

ABSTRACT: Natural genetic variation reveals key features of epigenetic and transcriptional memory in virus-specific CD8 T cells

PROVIDER: PRJNA523232 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8591830_1.fastq.gz	Fastqsanger.gz
	SRR8591830_2.fastq.gz	Fastqsanger.gz
	SRR8591840_1.fastq.gz	Fastqsanger.gz
	SRR8591840_2.fastq.gz	Fastqsanger.gz
	SRR8591850_1.fastq.gz	Fastqsanger.gz

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Natural genetic variation reveals key features of epigenetic and transcriptional memory in virus-specific CD8 T cells

Project description:Stable changes in chromatin states and gene expression in cells of the immune system form the basis for their memory of infections and other challenges. We used naturally occurring cis-regulatory variation in wild-derived inbred mouse strains to explore the mechanisms underlying long-lasting vs. transient gene regulation in antigen-specific CD8 T cells responding to acute viral infection. Our observations provide novel insights into the mechanisms driving stable and reversible transcriptional and epigenetic memory in virus-specific CD8 T cells. These findings suggest a general mechanism for the formation of epigenetic memory in CD8 T cells and other immune and non-immune cells.

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Natural Genetic Variation Reveals Key Features of Epigenetic and Transcriptional Memory in Virus-Specific CD8 T Cells.

Project description:Stable changes in chromatin states and gene expression in cells of the immune system form the basis for memory of infections and other challenges. Here, we used naturally occurring cis-regulatory variation in wild-derived inbred mouse strains to explore the mechanisms underlying long-lasting versus transient gene regulation in CD8 T cells responding to acute viral infection. Stably responsive DNA elements were characterized by dramatic and congruent chromatin remodeling events affecting multiple neighboring sites and required distinct transcription factor (TF) binding motifs for their accessibility. Specifically, we found that cooperative recruitment of T-box and Runx family transcription factors to shared targets mediated stable chromatin remodeling upon T cell activation. Our observations provide insights into the molecular mechanisms driving virus-specific CD8 T cell responses and suggest a general mechanism for the formation of transcriptional and epigenetic memory applicable to other immune and non-immune cells.

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Project description:Tissue health is dictated by the capacity to respond to perturbations and then return to homeostasis. Mechanisms that initiate, maintain, and regulate immune responses in tissues are therefore essential. Adaptive immunity plays a key role in these responses, with memory and tissue-residency being cardinal features. A corresponding role for innate cells is unknown. Here we have identified a population of innate lymphocytes that we term tissue-resident memory-like natural killer (NKRM) cells. In response to murine cytomegalovirus infection, we show that circulating NK cells were recruited in a CX3CR1-dependent manner to the salivary glands where they formed NKRM cells, a long-lived tissue-resident population that prevented autoimmunity via TRAIL-dependent elimination of CD4+ T cells. Thus, NK cells develop adaptive-like features, including long-term residency in nonlymphoid tissues, to modulate inflammation, restore immune equilibrium and preserve tissue health. Modulating the functions of NKRM cells may provide additional strategies to treat inflammatory and autoimmune diseases.

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