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ABSTRACT: MCMV-experienced ILC1 acquire an m12-dependent memory response

PROVIDER: PRJNA528997 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8784930_1.fastq.gz	Fastqsanger.gz
	SRR8784930_2.fastq.gz	Fastqsanger.gz
	SRR8784931_1.fastq.gz	Fastqsanger.gz
	SRR8784931_2.fastq.gz	Fastqsanger.gz
	SRR8784932_1.fastq.gz	Fastqsanger.gz

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MCMV-experienced ILC1 acquire an m12-dependent memory response

Project description:Innate and adaptive immune cells can acquire “memory” of encounters with a diverse range of activating signals to tune their response to secondary stimuli. Group 1 innate lymphoid cells (ILC1) are recently discovered tissue-resident sentinels that are essential for early host protection from intracellular pathogens at initial sites of infection. However, whether ILC1 function as short-lived effectors or persist and refine their responsiveness following pathogen challenge is not well understood. Furthermore, whether pathogen-derived antigens directly modulate tissue-resident ILC responses remains unclear. Here, we found that liver-resident ILC1 expand locally and persist following the resolution of mouse cytomegalovirus (MCMV) infection. MCMVexperienced ILC1 acquired stable transcriptional, epigenetic, and phenotypic changes, with an enhanced protective effector response to secondary MCMV challenge. Protective memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, but not formed during bystander cytokine activation following heterologous infection. Thus, liver ILC1 acquire adaptive features in a MCMV-specific manner.

2019-05-02 | GSE128906 | GEO

ILC1 confer early host protection at initial sites of viral infection [ATAC-Seq]

Project description:We show that tissue-resident ILC1 serve a non-redundant early role in host immunity through rapid production of interferon (IFN)-γ following mouse cytomegalovirus (MCMV) infection.

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Effector differentiation downstream of lineage commitment in ILC1 is driven by Hobit across tissues.

Project description:Innate lymphoid cells (ILCs) mediate early immunity against infection and participate in tissue inflammation and homeostasis. It is unclear how ILCs acquire effector function, and whether these mechanisms differ between organs. Through multiplexed single-cell mRNA-sequencing we identified cKit+CD127hiTCF-1hi early differentiation stages of T-bet+ ILC1. These cells were present across different organs and had the potential to mature towards CD127intTCF-1int and CD127-TCF-1- ILC1. Paralleling a gradual loss of TCF-1, differentiating ILC1 forfeited their expansion potential while increasing expression of effector molecules, reminiscent of T cell differentiation in secondary lymphoid organs. The transcription factor Hobit was induced in TCF-1hi ILC1s and was required for their effector differentiation. These findings reveal sequential mechanisms of ILC1 lineage commitment and ILC1 effector differentiation that are conserved across tissues. Our analyses suggest that ILC1 emerge as TCF-1hi cells in the periphery and acquire a spectrum of organ-specific effector phenotypes through a uniform Hobit-dependent differentiation pathway driven by local cues.

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ILC1 confer early host protection at initial sites of viral infection [RNA-Seq]

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EOMES interacts with RUNX3 and BRG1 to promote innate memory cell formation through epigenetic reprogramming

Project description:Memory CD8+ T cells have the ability to provide lifelong immunity against pathogens. Although memory features generally arise after challenge with a foreign antigen, naïve CD8 single positive (SP) thymocytes may acquire phenotypic and functional characteristics of memory cells in response to cytokines such as interleukin-4. This process is associated with the induction of the T-box transcription factor Eomesodermin (EOMES). However, the underlying molecular mechanisms remain ill-defined. Using epigenomic profiling, we show that these innate memory CD8SP cells acquire only a portion of the active enhancer repertoire of conventional memory cells. This reprograming is secondary to EOMES recruitment, mostly to RUNX3-bound enhancers. Furthermore, EOMES is found within chromatin-associated complexes containing BRG1 and promotes the recruitment of this chromatin remodelling factor. Also, the in vivo acquisition of EOMES-dependent program is BRG1-dependent. In conclusion, our results support a strong epigenetic basis for the EOMES-driven establishment of CD8+ T cell innate memory program.

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mRNA sequencing data of pancreatic cancer tumor tissues

Project description:We report the gene expression pattern of 125 pancreatic cancer tumor tissues who underwent surgical resectionmouse with IL-15, MCMV-infected mouse without IL-15, and MCMV-infected mouse with IL-15). We found that mouse with MCMV-memory CD8 T cells response to IL-15 and the behaviors of cancer were changed compared to other groups.

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Project description:Upon viral infection, NK cells expressing certain germline-encoded receptors are selected, expanded and maintained in an adaptive-like manner. Currently, these are thought to differentiate along a common pathway. However, by fate mapping of single NK cells upon murine cytomegalovirus (MCMV) infection, we identified two distinct NK cell lineages that contributed to adaptive-like responses. One was equivalent to conventional NK (cNK) cells while the other was transcriptionally similar to type 1 innate lymphoid cells (ILC1s). ILC1-like NK cells showed splenic-residency and strong cytokine production but also recognized and killed MCMV-infected cells, guided by activating receptor Ly49H. Moreover, they induced clustering of conventional type 1 dendritic cells and facilitated antigen-specific T cell priming early during MCMV infection, which depended on Ly49H and the NK cell-intrinsic expression of transcription factor Batf3. Thereby, ILC1-like NK cells bridge innate and adaptive viral recognition and unite critical features of cNK cells and ILC1s.

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