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DNA:RNA ImmunoPrecipitation (DRIP) sequencing data of virtual memory T cells In vitro induced from WT and Dusp2-/- CD8+ T cells

ABSTRACT: Virtual memory CD8+ T (TVM) cells are a distinct subset of antigen-inexperienced cells with rapid effector potential, but their regulatory checkpoints remain elusive. Here, using DRIP sequencing, we found that loss of DUSP2 promotes aberrant R-loop accumulation, leading to enhanced chromatin accessibility and subsequent TVM cell differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE329041 | GEO | 2026/04/29

REPOSITORIES: GEO

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RNA-seq data of virtual memory T cells In vitro induced from WT and DUSP2-/- CD8+ T cells

Project description:Virtual memory CD8+ T (TVM) cells are a distinct subset of antigen-inexperienced cells with rapid effector potential, but their regulatory checkpoints remain elusive. Here, using bulk RNA sequencing, we found that DUSP2 intrinsically limits the differentiation of highly activated TVM cells, thereby constraining antiviral immunity.

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Project description:A primary immune response is typically initiated in secondary lymphoid organs. Virtual memory CD8+ T (TVM) cells are antigen-inexperienced T cells of a central-memory phenotype, acquired through self antigen-driven homeostatic proliferation. Unexpectedly, here we find that, TVM cells are composed of CCR2+ and CCR2- subsets that differentially elaborate a spectrum of effector- and memory-poised functions directly in the tissue. During a primary flu infection, TVM cells rapidly infiltrate the lung in the first day and execute early viral control. TVM cells that recognize viral antigen are retained in the tissue, clonally expand independent of secondary lymphoid organs, and preferentially give rise to tissue-resident memory cells. By orchestrating an extra-lymphoid primary response, heterogenous TVM cells bridge innate reaction and adaptive memory directly in the infected tissue.

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DNA:RNA ImmunoPrecipitation (DRIP) sequencing data of virtual memory T cells In vitro induced from WT and Dusp2-/- CD8+ T cells

Project description:DNA:RNA ImmunoPrecipitation (DRIP) sequencing data of virtual memory T cells In vitro induced from WT and Dusp2-/- CD8+ T cells

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Project description:Virtual memory CD8+ T (TVM) cells provide rapid bystander protection during an infection despite their antigen naivety. In addition, these cells are also capable of antigen-specific response, making them an intriguing part of both the host innate and adaptive immune repertoire. While the innate and adaptive capabilities of these cells have been well characterized, much remains to be defined regarding the mechanisms governing their differentiation and function. Here, we investigate the role of the Ikaros zinc-finger (IkZF) transcription factor Aiolos in regulating CD8+ TVM generation and function. Using bulk RNA-sequencing and Assay for Transposase-Accessible Chromatin (ATAC)-sequencing, we identify differences in gene expression as well as accessibility profiles of key TVM effectors and regulators in TVM cells isolated from the spleen of control (wild-type) and Aiolos-deficient (Ikzf3-/-) mice. These studies will provide mechanistic insight into the regulation of TVM differentiation and function by Aiolos.

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Effect of Aiolos on virtual memory T cell differentiation and function [RNA-Seq]

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A distinct CD8+ T cell subset derived from virtual memory T cells causes alopecia areata through innate-like cytotoxicity [scRNA-seq]

Project description:Virtual memory T (TVM) cells are a T-cell subtype that exhibit a memory phenotype without prior exposure to a foreign antigen. Although several recent studies suggest that TVM cells exert anti-viral and anti-bacterial function, pathological roles of TVM cells causing inflammatory diseases have not been studied. Here, we identified a novel CD8+ T-cell subset (CD44s-hiCD49dlo CD8+ T cells), which is originated from TVM cells and can cause a chronic inflammatory disease, alopecia areata (AA). In the skin of alopecic mice, we detected a distinct TVM-cell subpopulation characterized by superior expression of CD44 and features of tissue residency, which was transcriptionally, phenotypically, and functionally distinct from conventional CD8+ TVM cells. Mechanistically, this cell population could be induced from conventional TVM cells by IL-12, IL-15, and IL-18 stimulation. Moreover, the pathological activity of CD44s-hiCD49dlo CD8+ T cells was mediated by NKG2D-depedent innate-like cytotoxicity against target cells, which was further augmented by IL-15 stimulation and triggered the onset of disease. Collectively, our results suggest a new immunological mechanism through which TVM cells can cause chronic inflammatory disease by innate-like cytotoxicity.

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