Characterization of CD8+ virtual memory T cells in IL-4 knockout mice using single-cell RNA sequencing
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ABSTRACT:
PROVIDER: PRJNA1146335 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30184501.fastq.gz | Fastqsanger.gz | |||
| SRR30184502.fastq.gz | Fastqsanger.gz |
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Project description:We profiled the heterogeneity of virtual memory T cells and observed changes in virtual memory T cell subsets under conditions of IL-4 deficiency in mouse spleens using single-cell RNA sequencing.
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Project description:The development of virtual memory CD8 T cells is dependent on IL-4, type I interferon, and IL-15. However, it remains unclear whether these cytokines individually contribute to the generation of specific subsets of virtual memory CD8 T cells. In this study, virtual memory CD8 T cells were categorized into four subsets based on Ly6C and Sca-1 expression, and their development was examined using knock-out mice lacking IFNAR1, IL-4, or IL-15Rα. Notably, both Ly6C+ Sca-1+ and Ly6C- Sca-1+ subsets were significantly reduced in the spleen of IFNAR1 knock-out mice, while the proportion of Ly6C+ Sca-1- VM CD8 T cells was reduced in IL-4-deficient mice. In IL-15Rα knock-out mice, both the Ly6C+ Sca-1- and Ly6C- Sca-1- subsets were significantly reduced. Bulk RNA sequencing analysis revealed distinct gene expression patterns in naïve cells, true memory cells, and four virtual memory cells subsets. Specifically, Ly6C+ subsets were enriched with IL-15 signal-related genes, whereas Ly6C- subsets and true memory cells were enriched for cell cycle-related genes. Functionally, the Ly6C+ subsets exhibited higher production of IFN-γ, TNF-α, and perforin compared to the Ly6C- subsets. Overall, this study demonstrates the heterogeneity of virtual memory CD8 T cells and highlights the cytokine-dependent nature for their development.
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Project description:Virtual memory (VM) CD8+ T cells are cytokine-driven, memory-phenotype lymphocytes maintained independently of antigen exposure. However, their role in chronic hepatic inflammation remains poorly defined. Here, we examined whether signaling through the IL-15/Rα complex (IL-15C) modulates VM CD8+ T cell responses during chronic liver injury. Mice were pretreated with IL-15C prior to induction of chronic liver injury using thioacetamide (TAA). VM CD8+ phenotypes, transcriptional profiles, and hepatic accumulation were analyzed by flow cytometry and mRNA sequencing. Type I interferon-deficient and CD8-depleted mouse model were used to assess the contribution of cytokine signaling and CD8+ T cells to the observed responses. IL-15C induced robust expansion of VM CD8+ T cells in both the spleen and liver, with preferential enrichment of a Ly6C+Sca-1+ subsets. IL-15C reprogrammed VM CD8+ T cells toward an effector and migratory phenotype, characterized by increased expression of EOMES, T-bet, NKG2D, and inflammatory chemokine receptors, along with reduced tissue-residency signatures. During chronic TAA-induced liver inflammation, VM CD8+ T cells, particularly the Ly6C+Sca-1+ subsets, accumulated in the liver, and IL-15C pretreatment further enhanced hepatic immune cell infiltration and was associated with sustained liver injury and fibrotic responses. Notably, IL-15-induced VM T cells exhibited reduced PD-1 expression and sustained NKG2D expression, especially within CD62L+ and CD69+ VM T cell populations. These findings demonstrate that IL-15C drives the expansion and phenotypic reprogramming of VM CD8+ T cells toward an effector-like, migratory state and is associated with enhanced hepatic immune cell infiltration during chronic liver injury.
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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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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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