Expression data from in vitro polarized-pathogenic Th17 system transfected with YY1 shRNA lentivirus
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PROVIDER: PRJNA767313 | ENA |
REPOSITORIES: ENA
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Project description:The proportion of pathogenic Th17 (pTh17) cells were significantly higher in RA than that in control individuals and showed a potential relevance with YY1 expression. Increased YY1 expression was observed in pTh17, and the pTh17 differentiation was hampered by YY1 knockdown. We used microarrays to detail the gene expression changes of pTh17 transfected with YY1 shRNA lentivirus and tried to elucidate the potential mechanisms how YY1 can affect pTh17 cell differentiation in RA.
2021-09-30 | GSE184979 | GEO
Project description:YY1 is a ubiquitously expressed, intrinsically disordered transcription factor involved in neural development. The oligomeric state of YY1 varies depending on the environment. These changes may alter its DNA binding ability and hence its transcriptional activity. In addition to its oligomeric state, the interaction of YY1 with proteins such as FOXP2 can impact its role in transcription. The aim of this work is to study the structure and dynamics of YY1 binding to DNA and to determine the influence of oligomerisation and associations with FOXP2 on its DNA binding mechanism. Size exclusion chromatography, fluorescence anisotropy and electrophoretic mobility shift assays were used to study YY1 oligomerisation and interaction with FOXP2. To better understand potential structural changes to YY1 upon DNA binding, hydrogen deuterium exchange mass spectrometry was used. The results indicate that YY1 consists of specific structured regions, while most of the sequence remains disordered. Furthermore, the oligomeric nature of the protein is dependent on ionic strength. DNA affects oligomerisation and the protein undergoes changes in structure and dynamics upon DNA binding. YY1 and FOXP2 were found to interact with each other both in isolation and in the presence of YY1-specific DNA. The heterogeneous, dynamic multimerisation of YY1 identified in this work is, therefore, likely to be important for its ability to make heterologous associations with other proteins such as FOXP2. The interactions that YY1 forms with itself, FOXP2 and DNA form part of an intricate mechanism of transcriptional regulation by YY1, which is vital for appropriate neural development.
2024-01-26 | PXD038431 | Pride
Project description:CD4+ T cells can differentiate into multiple effector subsets but the potential roles of these subsets in anti-tumor immunity have not been fully explored. We sought to study the impact of CD4+ T cell polarization on efficacy of tumor rejection in a model closely mimicking human disease where the target antigens are often non-mutated tissue differentiation self-antigens. We generated a new transgenic mouse model in which CD4+ T cells recognize a novel epitope in tyrosinase-related protein 1 (TRP-1), an antigen that is expressed by normal melanocytes and B16 murine melanoma. We found that cells could be robustly polarized into Th0, Th1 and Th17 subtypes in vitro, as evidenced by cytokine, chemokine, and adhesion molecule profiles as well as by surface markers, suggesting the potential for differential effector function in vivo. Contrary to the current view that Th1 cells play the most important role in tumor rejection, we found that Th17-polarized cells were superior in mediating destruction of advanced B16 melanoma. Unexpectedly, their therapeutic effect was critically dependent on IFN-γ production, while depletion of IL-17A and IL-23 had little impact. Taken together, these data indicate that the appropriate in vitro polarization of effector CD4+ T cells is decisive for the successful tumor eradication. This principle should be taken under consideration in the design of future clinical trials involving adoptive transfer-based immunotherapy of human malignancies. Two-condition experiment: RNA from TRP-1 transgenic mouse lymphocytes polarized to be either Th1 or Th17 were compared to cells polarized to be Th0. Keywords: Lymphocyte polarization comparison Comparative analysis of gene expression changes observed when murine lymphocytes are differentially in vitro polarized .
2010-05-25 | E-GEOD-10814 | biostudies-arrayexpress
Project description:HIV causes chronic inflammation and AIDS in humans, though the rate of disease progression varies between individuals. Similarly, simian lentiviruses vary in their pathogenicity based on characteristics of both the host (simian species) and virus strain. Here, we profile immune responses in pig-tailed macaques infected with variants of SIV that differ in virulence to understand the immune mechanisms underlying lentiviral pathogenicity. Compared to a minimally pathogenic lentiviral variant, infection with a highly pathogenic variant results in a more delayed, broad, and sustained activation of inflammatory pathways, including an extensive global interferon signature. Conversely, individual cells infected with highly pathogenic lentivirus upregulated fewer interferon-stimulated genes at a lower magnitude, indicating that highly pathogenic lentivirus has evolved to partially escape from interferon responses. Further, we identified distinct gene co-expression patterns and cell-cell communication pathways that implicate CXCL10 and CXCL16 as important molecular drivers of inflammatory pathways specifically in response to highly pathogenic lentivirus infection. Immune responses to highly pathogenic lentivirus infection are characterized by amplifying regulatory circuits of pro-inflammatory cytokines with dense longitudinal connectivity. Our work presents a model of lentiviral pathogenicity where failures in early viral control mechanisms lead to delayed, sustained, and amplifying pro-inflammatory circuits, which has implications for other viral infections with highly variable disease courses.
2024-01-17 | GSE228688 | GEO
Project description:Yin Yang 1 (YY1) is a multifunctional transcription factor with critical roles in carcinogenesis and metastasis. However, its biological role and clinical impact in colorectal cancer (CRC) remain unclear. This study aimed to elucidate the oncological role of YY1 in CRC. To indentify the target genes of YY1, microarray analysis was performed on siYY1 and siControl transfected cells.
2022-01-19 | GSE193949 | GEO
Project description:Tumor-associated macrophages are mainly polarized into the M2 phenotype, which remodels the tumor microenvironment and promotes tumor progression by secreting various cytokines. Herein, we reported that Yin Yang 1 (YY1) was highly expressed on tumor-infiltrated M2 macrophages in prostate cancer and was associated with poorer clinical outcomes. Using transgenic mice overexpressing YY1, we found that the tumor-promoting effects of oe-YY1 mice could be suppressed by macrophage depletion. Further in-vitro and in-vivo experiments using YY1 overexpressing and knocked down M2 macrophages demonstrated that YY1 induced M2 polarization and increased macrophages-induced prostate cancer progression by the IL-6/STAT3 pathway. Furthermore, YY1 promoted phase-separated condensates and upregulated IL-6 by modulating p300, p300 and CEBPB as a transcription complex. By conducting chromatin immunoprecipitation sequencing of M2 macrophages and monocytes, an M2-specific IL-6 enhancer associated with the YY1 complex was shown to upregulate IL-6 expression in M2 macrophages, and H3K27ac and YY1 signals significantly increased around this enhancer. In conclusion, YY1 complex promotes the M2 macrophages polarization and upregulates IL-6 in macrophages by inducing phase separation and a M2-specific enhancer, thereby increasing prostate cancer progression. These findings might lead to novel therapies targeting YY1 in prostate tumor-associated macrophages.
2023-04-01 | GSE200948 | GEO
Project description:Tumor-associated macrophages are mainly polarized into the M2 phenotype, which remodels the tumor microenvironment and promotes tumor progression by secreting various cytokines. Herein, we reported that Yin Yang 1 (YY1) was highly expressed on tumor-infiltrated M2 macrophages in prostate cancer and was associated with poorer clinical outcomes. Using transgenic mice overexpressing YY1, we found that the tumor-promoting effects of oe-YY1 mice could be suppressed by macrophage depletion. Further in-vitro and in-vivo experiments using YY1 overexpressing and knocked down M2 macrophages demonstrated that YY1 induced M2 polarization and increased macrophages-induced prostate cancer progression by the IL-6/STAT3 pathway. Furthermore, YY1 promoted phase-separated condensates and upregulated IL-6 by modulating p300, NF-κB and CEBPB as a transcription complex. By conducting chromatin immunoprecipitation sequencing of M2 macrophages and monocytes, an M2-specific IL-6 enhancer associated with the YY1 complex was shown to upregulate IL-6 expression in M2 macrophages, and H3K27ac and YY1 signals significantly increased around this enhancer. In conclusion, YY1 complex promotes the M2 macrophages polarization and upregulates IL-6 in macrophages by inducing phase separation and a M2-specific enhancer, thereby increasing prostate cancer progression. These findings might lead to novel therapies targeting YY1 in prostate tumor-associated macrophages.
2023-04-01 | GSE200947 | GEO
Project description:CD4+ T cells can differentiate into multiple effector subsets but the potential roles of these subsets in anti-tumor immunity have not been fully explored. We sought to study the impact of CD4+ T cell polarization on efficacy of tumor rejection in a model closely mimicking human disease where the target antigens are often non-mutated tissue differentiation self-antigens. We generated a new transgenic mouse model in which CD4+ T cells recognize a novel epitope in tyrosinase-related protein 1 (TRP-1), an antigen that is expressed by normal melanocytes and B16 murine melanoma. We found that cells could be robustly polarized into Th0, Th1 and Th17 subtypes in vitro, as evidenced by cytokine, chemokine, and adhesion molecule profiles as well as by surface markers, suggesting the potential for differential effector function in vivo. Contrary to the current view that Th1 cells play the most important role in tumor rejection, we found that Th17-polarized cells were superior in mediating destruction of advanced B16 melanoma. Unexpectedly, their therapeutic effect was critically dependent on IFN-γ production, while depletion of IL-17A and IL-23 had little impact. Taken together, these data indicate that the appropriate in vitro polarization of effector CD4+ T cells is decisive for the successful tumor eradication. This principle should be taken under consideration in the design of future clinical trials involving adoptive transfer-based immunotherapy of human malignancies. Two-condition experiment: RNA from TRP-1 transgenic mouse lymphocytes polarized to be either Th1 or Th17 were compared to cells polarized to be Th0. Keywords: Lymphocyte polarization comparison
2008-03-15 | GSE10814 | GEO
Project description:Yin Yang 1 (YY1) is a multifunctional transcription factor with critical roles in carcinogenesis and metastasis. However, its biological role and clinical impact in colorectal cancer (CRC) remain unclear. This study aimed to elucidate the oncological role of YY1 in CRC. To indentify the target genes of YY1, microarray analysis was performed on siYY1 and siControl transfected cells.
2022-01-19 | GSE193948 | GEO
Project description:These data include the genome wide location analyses of Yy1 by bioChIPs of Fbio-Yy1. Streptavidin precipitation of formaldehyde cross-linked chromatin prepared from Fbio-Yy1 and control expressing mouse ES cells
2012-01-04 | E-GEOD-31785 | biostudies-arrayexpress