MRNA exrpession from human gdT-cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE85482 | GEO | 2016/12/10
SECONDARY ACCESSION(S): PRJNA338621
REPOSITORIES: GEO
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Project description:Gamma-delta (gd) T cells from pooled mouse lymph nodes and spleens were isolated and FACS-sorted for Vg1+Ly6C-, Vg1+Ly6C+, Vg4+Ly6C- and Vg4+Ly6C+ subsets of bulk CD27+ gdT cells.
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Project description:Mus musculus isolate:gdT cells Raw sequence reads
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Project description:The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation. The molecular basis of this bi-directional communication remains to be fully elucidated. We use thermogenic adipose tissue as a model system to show that T cells, specifically gdT cells, play a critical role in promoting sympathetic innervation, at least in part through driving TGFβ1 expression in parenchymal cells via IL-17 Receptor C. Adipose-specific ablation of IL-17 Receptor C reduces TGFβ1 expression in adipocytes, impairs local sympathetic innervation and causes obesity and other metabolic phenotypes consistent with defective thermogenesis; innervation can be fully rescued by restoring TGFβ1 expression. Ablating gdT cells and the IL-17 Receptor C signaling pathway also impairs sympathetic innervation in salivary glands and the lung. These findings demonstrate T cell/parenchymal cell coordination to regulate sympathetic innervation.
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Project description:We utilized RNA-seq to identify differential gene expression in Vγ9 Vδ2 gdT cells isolated from human PBMCs upon TCR stimulation. We find that ~30% genes are commonly up- and down-regulated between different phosphoantigen treatments (p<0.05). Inhibition of Notch signaling alongside TCR activation results in downregulation of many effector genes in Vγ9 Vδ2 T cells.
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Project description:Innate-like gd T effector subsets are exported from the thymus as “memory-like” cells prewired for rapid, specialized function. Previously, we showed that emergent gd subsets distinguished by TCRg and TCRd usage in the fetal and adult thymus possess distinct global transcriptomes and the subset-specific combinatorial expression of High Mobility Group box transcription factors (HMG TFs) shown as a primary determinant of gd effector differentiation. While the detailed mechanism of HMG TFs cooperativity and counter-regulations are not fully understood, a key feature for IL-17 producing gd T effectors (Tgd17) is predicted to be context-dependent interactions between SOX13 and TCF1 that result in diversified target gene regulation. More SOX13 allow more TCF1 dockings on DNA. TCF1 chromatin occupancy in the Tgd17 gene cluster (V2 set) mimics when the amount of SOX13 is enhanced like the Sox13 transgenic system. Globally 75% of SOX13 binding is overlapped with TCF1 binding and V2 set-specifically 85% of SOX13 targets are overlapped with TCF1 targets. The genome-wide analysis between TCF1 and SOX13 indicates cooperative and active SOX13-dependent-TCF1-modulations on V2 sets.
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Project description:Innate-like gd T effector subsets are exported from the thymus as “memory-like” cells prewired for rapid, specialized function. Previously, we showed that emergent gd subsets distinguished by TCRg and TCRd usage in the fetal and adult thymus possess distinct global transcriptomes and the subset-specific combinatorial expression of High Mobility Group box transcription factors (HMG TFs) shown as a primary determinant of gd effector differentiation. While the detailed mechanism of HMG TFs cooperativity and counter-regulations are not fully understood, a key feature for IL-17 producing gd T effectors (Tgd17) is predicted to be context-dependent interactions between SOX13 and TCF1 that result in diversified target gene regulation. More SOX13 allow more TCF1 dockings on DNA. TCF1 chromatin occupancy in the Tgd17 gene cluster (V2 set) mimics when the amount of SOX13 is enhanced like the Sox13 transgenic system. Globally 75% of SOX13 binding is overlapped with TCF1 binding and V2 set-specifically 85% of SOX13 targets are overlapped with TCF1 targets. The genome-wide analysis between TCF1 and SOX13 indicates cooperative and active SOX13-dependent-TCF1-modulations on V2 sets.
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Project description:Injuries to the retinal pigment epithelium (RPE) and outer retina often result in the accumulation of retinal microglia within the subretinal space. These subretinal microglia play crucial roles in inflammation and resolution, but the mechanisms governing their functions are still largely unknown. Our previous research highlighted the protective functions of choroidal gd T cells in response to RPE injury. In the current study, we employed single-cell RNA sequencing approach to delve deeper into the mechanisms involved. We found that gd T cells were the primary producer of interleukin-17 (IL-17) in the choroid. IL-17 signaled through its receptor on the RPE, subsequently triggering the production of interleukin-6 (IL-6). This cascade of cytokines initiated a metabolic reprogramming of subretinal microglia, enhancing their capacity for lipid metabolism. RPE-specific knockout of IL-17 receptor A led to the dysfunction of subretinal microglia and RPE pathology. Collectively, our findings suggest that responding to RPE injury, the choroidal gd T cells can initiate a protective signaling cascade that ensures the proper functioning of subretinal microglia.
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Project description:Our team had previously explored the potential of expanding cord blood (CB) derived γδ T cells (CB-gdT) as well as their corresponding ability to target primary acute myeloid leukemia (AML) cells. Using a feeder cell line-based in vitro expansion protocol, we achieved a clinically relevant scale expansion of γδ T cells over a period of 14 days. These cells exhibit variable degree of potency against a range of human AML cell lines and primary patient samples. In order to dissect the cellular and molecular programs governing the activation, differentiation and functional states of our in vitro expanded CB-gdT, we performed multiplex single cell sequencing analysis using the 10X Genomics Chromium System. After initial quality check and filtering, data from a total of 4,276 cells were retrieved. Among which, we identified 742 unique TCRγδ clonotypes, representing 18.6% of the starting 4,000 FACS purified γδ T cells seeded for expansion. Consistent to our FACS analysis, Vδ1 is the predominant TRD chain in the expanded cultures, accounting for 61.2% of all clones. Based on uniform manifold approximation and projection for dimension reduction (UMAP), all cells were clustered into 11 subsets. Key cytotoxic genes including GZMB, GZMA and NKG7 were all highly expressed across all clusters, indicating that the expanded cells were indeed functionally cytotoxic. Comparing against multiple curated gene sets, we have identified 3 main subsets of γδ T cells: the Proliferative, Cytotoxic γδ T cells (P-CT), Differentiated Cytotoxic γδ T cells (D-CT) and Late Activated Cytotoxic γδ T cells (LA-CT). P-CT (~46% of all cells) shows an expression profile positively associated with cell proliferation as well as increased cell surface expression of memory T cell markers CD27, CCR7 and CD62L. Similar to cytotoxic genes, genes associated with TCR signaling and interferon response were found to be expressed across all cell clusters, yet with elevated levels in D-CT and LA-CT. Furthermore, cell surface expression of different NK receptors including NKG2D, DNAM1 and NKp30 are more enriched in LA-CT compared to the other 2 subsets, suggesting the acquisition of additional NK receptor related functions in this group of cells. Consistent with the concept of progressive γδ T cell differentiation and activation in culture, we found that in 85 (11.5%) of the γδ T cell clones bearing more than 10 cells each, all clones contain cells distributed across the 3 different γδ T cell subsets. This is the first report on single cell immune profiling of in vitro expanded gdT cells derived from human CB.
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Project description:Innate-like gd T effector subsets are exported from the thymus as “memory-like” cells prewired for rapid, specialized function. Previously, we showed that emergent gd subsets distinguished by TCRg and TCRd usage in the fetal and adult thymus possess distinct global transcriptomes and the subset-specific combinatorial expression of High Mobility Group box transcription factors (HMG TFs) shown as a primary determinant of gd effector differentiation. While the detailed mechanism of HMG TFs cooperativity and counter-regulations are not fully understood, a key feature for IL-17 producing gd T effectors (Tgd17) is predicted to be context-dependent interactions between SOX13 and TCF1 that result in diversified target gene regulation. More SOX13 allow more TCF1 dockings on DNA. TCF1 chromatin occupancy in the Tgd17 gene cluster (V2 set) mimics when the amount of SOX13 is enhanced like the Sox13 transgenic system. Globally 75% of SOX13 binding is overlapped with TCF1 binding and V2 set-specifically 85% of SOX13 targets are overlapped with TCF1 targets. Mostly V2 sets are H3K4me3 (79%) and the genome wide analysis between TCF1 and SOX13 indicate cooperative and active SOX13-dependent-TCF1-modulations on V2 sets.
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