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Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues

ABSTRACT: Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues

PROVIDER: PRJNA782679 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17011162.fastq.gz	Fastqsanger.gz
	SRR17011163.fastq.gz	Fastqsanger.gz
	SRR17012163.fastq.gz	Fastqsanger.gz
	SRR17011164.fastq.gz	Fastqsanger.gz
	SRR17012164.fastq.gz	Fastqsanger.gz

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Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues.

Project description:Regulatory T cells (Tregs) mediate immune homeostasis, yet also facilitate nuanced immune responses during infection, balancing pathogen control while limiting host inflammation. Recent studies have identified Treg populations in non-lymphoid tissues that are phenotypically distinct from Tregs in lymphoid tissues (LT), including performance of location-dependent roles. Mucosal tissues serve as critical barriers to microbes while performing unique physiologic functions, so we sought to identify distinct phenotypical and functional aspects of mucosal Tregs in the female reproductive tract. In healthy human and mouse vaginal mucosa, we found that Tregs are highly activated compared to blood or LT Tregs. To determine if this phenotype reflects acute activation or a general signature of vaginal tract (VT)-residency, we infected mice with HSV-2 to discover that VT Tregs express granzyme-B (GzmB) and acquire a VT Treg signature distinct from baseline. To determine the mechanisms that drive GzmB expression, we performed ex vivo assays to reveal that a combination of type-I interferons and interleukin-2 is sufficient for GzmB expression. Together, we highlight that VT Tregs are activated at steady state and become further activated in response to infection; thus, they may exert robust control of local immune responses, which could have implications for mucosal vaccine design.

| S-EPMC9391309 | biostudies-literature

Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues [bulk RNA-seq]

Project description:Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues [bulk RNA-seq]

| PRJNA782685 | ENA

Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues [single-cell RNA-seq]

Project description:Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues [single-cell RNA-seq]

| PRJNA782684 | ENA

Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues [bulk RNA-seq]

Project description:Vaginal tissue Tregs acquire a inflammatory cytokine-dependent, infection-specific phenotype after local infection with HSV-2

2022-04-15 | GSE189373 | GEO

Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues [single-cell RNA-seq]

Project description:Vaginal tissue Tregs acquire a inflammatory cytokine-dependent, infection-specific phenotype after local infection with HSV-2

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Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues

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

2022-04-15 | GSE189375 | GEO

Distinct murine mucosal Langerhans cell subsets develop from pre-DCs and monocytes

Project description:Langerhans cells (LCs) populate the mucosal epithelium, a major entry portal for pathogens, yet their ontogeny remains unclear. In contrast to skin LCs originating from self-renewing radioresistant embryonic precursors, we found that oral mucosal LCs derive from circulating radiosensitive precursors. Mucosal LCs can be segregated into CD103+CD11blow (CD103+LCs) and CD11b+CD103- (CD11b+LCs) subsets. We further demonstrated that similar to non-lymphoid dendritic cells (DCs), CD103+LCs originate from pre-DCs, whereas CD11b+LCs differentiate from both pre-DCs and monocytic precursors. Despite this ontogenetic discrepancy between skin and mucosal LCs, transcriptomic signature and immunological function of oral LCs highly resemble those of skin LCs but not DCs. These findings, along with their epithelial position, morphology and expression of LC-associated phenotype strongly suggest that oral mucosal LCs are genuine LCs. Collectively, in a tissue-dependent manner, murine LCs differentiate from at least three distinct precursors (embryonic, pre-DCs and monocytic) in steady state The following cells were isolated from mice (2-4 replicates): Lung DCs, mucosal CD103+ LC, mucosal CD11b+ LC, Skin LC. Transcriptome analysis was performed.

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Distinct murine mucosal Langerhans cell subsets develop from pre-DCs and monocytes

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Difference of LncRNAs expression between colorectal tumor tissues and paracancer normal intestinal mucosal tissues

Project description:To identify the difference of LncRNAs expression between colorectal tumor tissues and paracancer normal intestinal mucosal tissues

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Cohesin residency determines chromatin loop patterns

Project description:Cohesin residency determines chromatin loop patterns

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