Single-cell transcriptomic analysis of tissue resident memory T cells in human lung cancer [ bulk RNA-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE111892 | GEO | 2019/06/13
REPOSITORIES: GEO
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Project description:High numbers of tissue-resident memory T (TRM) cells have been associated with better clinical outcomes in cancer patients. However, the molecular characteristics that drive their efficient immune response to tumors are poorly understood. Here, using single-cell and bulk transcriptomic analysis of purified populations of TRM and non-TRM cells we characterise these populations
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Project description:Recirculating and tissue-resident memory CD8+ T cells provide distinct modes of immune protection, yet the signals that dictate differentiation of these populations are ill-defined. In particular, the interactions within tissues that promote generation of resident memory T cells (TRM) are unclear. Here, we show that the inducible costimulatory molecule ICOS, well known to regulate differentiation of CD4+ T cell populations, is required for CD8+ TRM but not recirculating memory subsets. Furthermore, ICOS engagement during CD8+ T cell recruitment to non-lymphoid tissues is critical for efficient TRM establishment: ICOS/ICOS-L interactions are dispensable throughout CD8+ T cell priming and for TRM maintenance, while ICOS-L expression by radioresistant cells is key for optimal TRM generation. This role for ICOS depends on its ability to signal through PI3K. Together, our data illustrate that specific local costimulatory cues promote production of tissue-resident populations, with potential implication for therapeutic manipulation.
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Project description:Purpose: To characterize the tumor-specific TRM cells in LNs, skin, lung and liver in mice with melanoma-associated vitiligo (MAV). Bulk RNA-seq was performed to identify populations of CD8 T cells with TRM transcriptional characteristics. Methods: CD8+THy1.1+ T cells were sorted from DLN, skin lung and liver of MAV mice and bulk RNA-sequenced Results: Heterogenouse CD8 memory populations with both circulatating and resident phenotypes were identified. Conclusions: Tumor-specific CD8 T cells form TRM responses in tumor-draining LNs.
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Project description:Tissue resident memory (Trm) represent a newly described memory T cell population. We have previously characterized a population of Trm that persists within the brain following acute virus infection. Although capable of providing marked protection against a subsequent local challenge, brain Trm do not undergo recall expansion following dissociation from the tissue. Furthermore, these Trm do not depend on the same survival factors as the circulating memory T cell pool as assessed either in vivo or in vitro. To gain greater insight into this population of cells we compared the gene-expression profiles of Trm isolated from the brain to circulating memory T cells isolated from the spleen following an acute virus infection. Trm displayed altered expression of genes involved in chemotaxis, expressed a distinct set of transcription factors and overexpressed several inhibitory receptors. Cumulatively, these data indicates that Trm are a distinct memory T cell population disconnected from the circulating memory T cell pool and displaying a unique molecular signature which likely results in optimal survival and function within their local environment. 13 samples were analyzed: 5 replicates of memory OT-I CD8+.CD103- T cells isolated from the spleen of mice on day 20 p.i. with VSV-OVA. 5 replicates of memory OT-I CD8+CD103+ T cells isolated from the brain of mice on day 20 p.i. with VSV-OVA; and 3 replicates of memory OT-I.CD8+ CD103- T cells isolated from the brain of mice on day 20 p.i. with VSV-OVA
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Project description:The networks of transcription factors (TFs) that control multipotency versus effector programs in intestinal resident memory T (TRM) cells are poorly understood. Mice with post-activation, conditional deletion of the TF Bcl11b in CD8+ T cells, infected with a food-born pathogen, had increased numbers of intestinal TRM cells, and their precursors and decreased splenic effector cells and circulating memory cells and precursors. Loss of circulating memory cells was in part due to increased intestinal homing of Bcl11b-/- circulating precursors with no major alterations in their programs. Bcl11b-/- memory CD8+ T cells had an impaired recall response despite their accumulation in the gut. Intestinal Bcl11b-/- TRM cells and their precursors manifested major alterations in the residency program, with diminished expression of multipotency program genes and upregulation of the effector program genes. Integration of transcriptomics with chromatin accessibility, activating histone marks and Bcl11b genome binding showed a link between the reduction in the multipotent program genes with regions of decreased chromatin accessibility and activating histone marks in Bcl11b-/- cells. In contrast, the effector program genes displayed increased activating epigenetic status. We propose that Bcl11b regulates tissue resident TRM program genes and is positioned upstream of Tcf1 and Blimp1 in regulation of multipotency versus effector TRM program, respectively. Rescuing experiments normalized the increased numbers of intestinal Bcl11b-/- TRM cells. Thus, Bcl11b is a frontrunner in the memory tissue residency program and acts early in lineage decision, promoting TRM cell multipotency and restricting effector function.
2023-06-09 | GSE222911 | GEO
Project description:The networks of transcription factors (TFs) that control multipotency versus effector programs in intestinal resident memory T (TRM) cells are poorly understood. Mice with post-activation, conditional deletion of the TF Bcl11b in CD8+ T cells, infected with a food-born pathogen, had increased numbers of intestinal TRM cells, and their precursors and decreased splenic effector cells and circulating memory cells and precursors. Loss of circulating memory cells was in part due to increased intestinal homing of Bcl11b-/- circulating precursors with no major alterations in their programs. Bcl11b-/- memory CD8+ T cells had an impaired recall response despite their accumulation in the gut. Intestinal Bcl11b-/- TRM cells and their precursors manifested major alterations in the residency program, with diminished expression of multipotency program genes and upregulation of the effector program genes. Integration of transcriptomics with chromatin accessibility, activating histone marks and Bcl11b genome binding showed a link between the reduction in the multipotent program genes with regions of decreased chromatin accessibility and activating histone marks in Bcl11b-/- cells. In contrast, the effector program genes displayed increased activating epigenetic status. We propose that Bcl11b regulates tissue resident TRM program genes and is positioned upstream of Tcf1 and Blimp1 in regulation of multipotency versus effector TRM program, respectively. Rescuing experiments normalized the increased numbers of intestinal Bcl11b-/- TRM cells. Thus, Bcl11b is a frontrunner in the memory tissue residency program and acts early in lineage decision, promoting TRM cell multipotency and restricting effector function.
2023-06-09 | GSE222914 | GEO
Project description:The networks of transcription factors (TFs) that control multipotency versus effector programs in intestinal resident memory T (TRM) cells are poorly understood. Mice with post-activation, conditional deletion of the TF Bcl11b in CD8+ T cells, infected with a food-born pathogen, had increased numbers of intestinal TRM cells, and their precursors and decreased splenic effector cells and circulating memory cells and precursors. Loss of circulating memory cells was in part due to increased intestinal homing of Bcl11b-/- circulating precursors with no major alterations in their programs. Bcl11b-/- memory CD8+ T cells had an impaired recall response despite their accumulation in the gut. Intestinal Bcl11b-/- TRM cells and their precursors manifested major alterations in the residency program, with diminished expression of multipotency program genes and upregulation of the effector program genes. Integration of transcriptomics with chromatin accessibility, activating histone marks and Bcl11b genome binding showed a link between the reduction in the multipotent program genes with regions of decreased chromatin accessibility and activating histone marks in Bcl11b-/- cells. In contrast, the effector program genes displayed increased activating epigenetic status. We propose that Bcl11b regulates tissue resident TRM program genes and is positioned upstream of Tcf1 and Blimp1 in regulation of multipotency versus effector TRM program, respectively. Rescuing experiments normalized the increased numbers of intestinal Bcl11b-/- TRM cells. Thus, Bcl11b is a frontrunner in the memory tissue residency program and acts early in lineage decision, promoting TRM cell multipotency and restricting effector function.
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