Ontology highlight
ABSTRACT:
PROVIDER: PRJNA873268 | ENA |
REPOSITORIES: ENA
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Project description:Papillary thyroid cancer (PTC) is the most common thyroid malignancy. Although PTC patients usually show a favorable prognosis, some still have a high rate of recurrence and a relatively low survival rate. We aimed to reveal the mechanisms involved in the development of thyroid cancer using single-cell RNA sequencing (scRNA-seq).scRNA-seq data was collected from 15 samples, including primary tumors of PTC, metastatic lymph nodes (LNs), and adjacent normal tissues. The results from scRNA-seq data were further validated with flow cytometry, proliferation, invasion, and migration assays, and bulk RNA-seq data.A novel CD4+T cell subset was identified, termed as EGR1+CD4+T cells. It produced high levels of IL-10 and IFN-γ in response to phorbol 12-myristate 13-acetate (PMA) and ionomycin, and showed a distinct molecular pathway activity compared to CD4+Tregs. CD4+T cell-specific over-expression of EGR1 in vitro enhanced tumor cell proliferation, invasion, and migration when co-cultured with PTC cell lines. The expression profiling analysis of immune checkpoint molecules indicated that CD96 was commonly up-regulated in EGR1+CD4+T cells, CD4+Tregs, and other T cell subsets, especially in tumor tissues. Single CD96 blockade significantly increased the levels of IFN-γ, IL-17a, and IL-10 in EGR1+CD4+T cells, and inhibited the proliferation of PTC tumor cells. Co-blockade of CD96/TIGIT significantly enhanced the production of IFN-γ, TNF-α, and IL-17a in both EGR1+CD4+T and CD3+CD4+T cells, which also suppressed cell proliferation, invasion, and migration when co-cultured with PTC tumor cells. These findings indicated that EGR1+CD4+T cell was a novel CD4+T cell subset with specific functions. Single CD96 blockade or co-blockade of CD96/TIGIT enhanced antitumor immunity of EGR1+CD4+T cells, which might be promising therapeutic strategies in PTC treatment.
2025-02-06 | GSE274674 | GEO
Project description:Cell culture conditions impact the clinical efficacy of chimeric antigen receptor (CAR) T cell products, but the optimal approach remains unknown. Separate CD4+ and CD8+ cultures offer a potential advantage but complicate manufacturing and may affect cell expansion and function. We evaluated the co-culture of CD4+ and CD8+ cells at a defined ratio at culture initiation. We observed that the presence of CD4+ cells markedly improves expansion of CD8+ CAR T cells, and CD8+ cells cultured in isolation exhibit a hypofunctional phenotype and transcriptional signature compared with those co-cultured with CD4+ cells. Mixed-culture CAR T cells also confer superior anti-tumor activity in vivo compared with separately expanded, co-infused cells. CD4+ cell effects on CD8+ cells are mediated through both cytokines and direct cell contact, including CD40L-CD40 and CD70-CD27 interactions.
2023-11-30 | GSE245427 | GEO
Project description:Extracellular vesicles (EVs) participate in cell-stroma crosstalk within tumor microenvironment (TME) and Fb are key elements that contribute to tumor promotion. In thyroid cancer, the most prevalent endocrine malignancy, the relevance of Fb in the TME and EVs is beginning to be deciphered. Using an in vitro model of tumor-stroma crosstalk, we performed the comparative proteomic analysis of EVs secreted in tumoral- and non-tumoral milieu to describe EV-functionality and examine their possible role in thyroid tumor progression-related events. Tumor (TPC-1, 8505c) or non-tumor (NThyOri) thyroid cells were co-cultured with human fibroblasts (Fb). EVs, obtained by ultracentrifugation of conditioned media (CMs), were characterized by mass-spectrometry.
2022-08-02 | PXD028081 | Pride
Project description:This study elucidates the effect of the E2F1-regulated melanoma-secreted factors on the phenotype and transcriptional program of immune cells (CD4+ T and CD8+ T cells) in the melanoma immune microenvironment. In order to determine the immune modulatory effect of the secretome on immune cells, we established a co-culture system where different melanoma cell lines (high-E2F1/invasive and low E2F1/non-invasive) were co-cultured with CD4+ or CD8+ T cells without direct interaction. These data describe the transcriptomes of immune cells and for the two melanoma cell lines Mel147 and C8161, both in co- and monoculture condition, with stable E2F1 knockdowns and corresponding controls.
2024-10-27 | E-MTAB-12750 | biostudies-arrayexpress
Project description:In Gravesâ?? disease (GD), a combination of genetic, epigenetic and environmental factors causes an autoimmune response to the thyroid gland, characterized by lymphocytic infiltrations and autoantibodies targeting the thyroid stimulating hormone receptor (TSHR) and other thyroid antigens. To identify the epigenetic changes involved in GD, we performed a genome-wide analysis of DNA methylation and enrichment of H3K4me3 and H3K27ac histone marks in sorted CD4+ and CD8+ T cells. We found 365 and 3322 differentially methylated CpG sites in CD4+ and CD8+ T cells, respectively. Among the hypermethylated CpG sites, we specifically found enrichment of genes involved in T cell signaling (CD247, LCK, ZAP70, CD3D, CD3E, CD3G, CTLA4 and CD8A) and decreased expression of CD3 gene family members. The hypermethylation was accompanied with the active chromatin histone modifications as we found decreased signals of H3K4me3 and H3K27ac marks at several T cell signaling genes in ChIP-seq analysis. In addition, we found hypermethylation of the TSHR gene first intron, where several GD-associated polymorphisms are located. Our results demonstrate an involvement of dysregulated DNA methylation and histone modifications at T cell signaling genes in GD patients. Individuals were recruited from the Estonian Genome Center of the University of Tartu. Genomic DNA was extracted from sorted CD4+ (H3K4me3 ChIP: 15 controls and 14 GD patients; H3K27ac ChIP: 11 controls and 13 GD patients) and CD8+ (H3K4me3 ChIP: 17 controls and 14 GD patients; H3K27ac ChIP: 15 controls and 14 GD patients) T cells. The data collection was performed at the SNP&SEQ Technology Platform in Uppsala University, and data analysis was done at the Institute of Biomedicine and Translational Medicine in the University of Tartu.
2015-11-06 | E-GEOD-71952 | biostudies-arrayexpress
Project description:PBMCs from healthy donor were co-cultured with the cell line PGA-1 and stimulated with anti-CD3/28 antibodies for 48 hours. CD4 T cells were then FACS sorted for RNA seq analysis
2023-08-31 | GSE226599 | GEO
Project description:Teff cells (CD4+CD25-CD127+CD45RO+) were co-cultured with and without sorted Treg subsets plus dendritic cells for 18h. All the sorted Teff cells are gated on CD4+CD25-CD127(hi), and further sorted for CD45RO- and CD45RO+ phenotype.
2015-10-01 | GSE64180 | GEO
Project description:RNA-sequencing data of 5 human thyroid cancer cell lines cultured in control conditions
| EGAD00001011677 | EGA
Project description:Comparison of gene expression by co-cultured WC1+ gammadelta and CD4+ alphabeta T cells
| PRJNA96889 | ENA
Project description:Tagged versions of thyroid hormone receptors alpha (TRa) and beta (TRb) were stably transfected in two C17.2 cell lines, C17.2a and C17.2b, respectively. We performed an affinity-based purification of chromatin (ChAP), and high-throughput sequencing was used to assess binding sites of both receptors (ChAP-Seq). Standard ChIP-Seq for RXR was also performed in C17.2a cells. These data allow us to compare binding sites for both receptors and to conclude that they were only partially redundant, with co-existence of receptor-specific sites. Examination of binding sites of the two thyroid hormone receptors (alpha, beta) in two cell lines (C17.2a, C17.2b), each expressing one of the receptors. Examination of RXR binding sites in C17.2a cells.
2012-12-31 | E-GEOD-38347 | biostudies-arrayexpress