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

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

PROVIDER: PRJNA782685 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17011162.fastq.gz	Fastqsanger.gz
	SRR17011163.fastq.gz	Fastqsanger.gz
	SRR17011164.fastq.gz	Fastqsanger.gz
	SRR17011165.fastq.gz	Fastqsanger.gz
	SRR17011166.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:Mucosal viral infection induces a regulatory T cell activation phenotype distinct from tissue residency in mouse and human tissues

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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

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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]

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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.

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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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