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Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma [RRBS]

ABSTRACT: PD-L1 is a ligand for the inhibitory PD1 receptor on T cells and its expression in some cancers inhibits anti-cancer immune response. In melanoma, PD-L1 expression is induced in response to immune stimuli but in a proportion of melanomas it is constitutively expressed. Factors that drive constitutive expression of PD-L1 are unknown. Here we performed genome-scale methylation analysis of six cell lines that constitutively express PD-L1 (PD-L1 positive, referred to as PD-L1CON) and six cell lines that only express PD-L1 after treatment with IFN- (PD-L1 negative, referred to as PD-L1IND)

ORGANISM(S): Homo sapiens

PROVIDER: GSE107621 | GEO | 2018/05/24

REPOSITORIES: GEO

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Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma [RNA-Seq]

Project description:PD-L1 is a ligand for the inhibitory PD1 receptor on T cells and its expression in some cancers inhibits anti-cancer immune response. In melanoma, PD-L1 expression is induced in response to immune stimuli but in a proportion of melanomas it is constitutively expressed. Factors that drive constitutive expression of PD-L1 are unknown. Here we performed RNA-Seq analysis of six cell lines that constitutively express PD-L1 (PD-L1 positive, referred to as PD-L1CON) and six cell lines that only express PD-L1 after treatment with IFN- (PD-L1 negative, referred to as PD-L1IND)

2018-05-24 | GSE107620 | GEO

Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma [RRBS]

Project description:Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma [RRBS]

| PRJNA420862 | ENA

Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma

Project description:Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma

| PRJNA420852 | ENA

Analysis of mouse T cell transcription profile after co-culture with BaF3 cells with or without the oncogenic point mutation JAK2 V617F

Project description:The activation of PD-1 (Programmed Death receptor-1) on T cells can cause T cell exhaustion and immune tolerance. Some tumors up-regulate the expression of the ligand of PD-1, namely PD-L1 (Programmed Death Receptor-Ligand 1), thus preventing anti-tumor immune response and promoting immune-escape. Previous studies have shown that JAK2 (Janus Kinase 2) signaling can promote PD-L1 expression in Hodgkin Lymphoma. In Myeloproliferative Neoplasms (MPN), JAK2 is frequently characterized by the the presence of the point-mutation V617F, which leads to its constitutive activation and to uncontrolled cell proliferation and survival. Accordingly, tumor cell lines expressing JAK2 V617F express higher levels of PD-L1 as compared to tumor cell lines negative for such mutations. In this experiment, we transfected BaF3 cells with a vector (plasmid for Murine Stem Cell Virus) containing the gene for JAK2 with the point-mutation V617F. As control, we used BaF3 cells transfected with the same vector, but without the gene for JAK2 V617F (empty vector). Both the cell lines (with/without JAK2 V617F) were co-cultured with primary murine T cells. When co-cultured with BaF3 cells expressing JAK2 V617F, T cells upregulated genes connected to senescence pathways, showed increased apoptosis, less cytokine production, and displayed other forms of dysfunction which can be associated with the activation of PD-1.

2018-12-01 | E-MTAB-5028 | biostudies-arrayexpress

Regulation of follicular T-helper cell positioning and function by PD-1

Project description:Follicular T-helper (TFH) cells highly express the programmed cell death-1 (PD-1) molecule. Whereas inhibition of T cell receptor (TCR) signaling and CD28 co-stimulation is thought to be the primary mode of PD-1 functions, how PD-1 regulates TFH development and function remains unclear. Here we show that, when engaged by the ensemble of bystander B cells constitutively expressing PD-1 ligand 1 (PD-L1), PD-1 inhibits T-cell recruitment into follicles. This inhibition involves suppression of PI3K activities downstream of follicle-guidance receptor CXCR5, is independent from co-signaling with the TCR, and necessitates ICOS signaling to overcome. PD-1 further restricts CXCR3 upregulation on TFH cells, serving to concentrate these cells toward the GC territory, where PD-L1-PD-1 interactions between individual TFH and B cells optimize B-cell competition and affinity maturation. Therefore, operating in both costimulation-independent and -dependent manners, PD-1 plays an integral role in orchestrating tissue positioning and function of TFH cells.

2018-08-30 | GSE112066 | GEO

Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma [RNA-Seq]

Project description:Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma [RNA-Seq]

| PRJNA420861 | ENA

Transcript data affected by constitutive expression of VvMYBPAR in Arabidopsis

Project description:Constitutive expression of VvMYBPAR in Arabidopsis was found to accumulate proanthocyanidins when the plants were grown on sucrose-supplemented media to induce anthocyanins. To identify the putative targets of VvMYBPAR, the transcriptome analysis of the transgenic lines which highly express VvMYBPAR was carried out using NimbleGen microarray. Three transgenic lines in which VvMYBPAR were constitutively expressed under the control of 35S promoter vs. empty vector transformants were compared.

2014-06-03 | E-GEOD-55318 | biostudies-arrayexpress

Enhancing PD-L1 Degradation by ITCH during MAPK Inhibitor Therapy Suppresses Acquired Resistance

Project description:Disrupting PD-1/PD-L1 interaction rejuvenates antitumor immunity. Clinical successes by blocking PD-1/PD-L1 binding have grown across wide-ranging cancer histologies, but innate therapy resistance is evident in the majority of treated patients1. Cancer cells can express robust surface levels of PD-L1 to tolerize tumor-specific T cells, but regulation of PD-L1 protein levels in the cancer cell is poorly understood. Quasi-mesenchymal tumor cells up-regulate PD-L1/L2 and induce an immune-suppressive microenvironment, including expansion of M2-like macrophages and regulatory T cells and exclusion of CD8+ T-cell infiltration2. Targeted therapy, including MAPK inhibitor therapy in melanoma, leads to quasi-mesenchymal transitions and resistance3, and both MAPK inhibitor treatment and mesenchymal signatures are associated with innate anti-PD-1 resistance4,5. Here we identify ITCH as an E3 ligase that downregulates tumor cell-surface PD-L1/L2 in PD-L1/L2-high cancer cells, including MAPK inhibitor-resistant melanoma, and suppresses acquired MAPK inhibitor resistance in and only in immune-competent mice. ITCH interacts with and poly-ubiquitinates PD-L1/L2, and ITCH deficiency increases cell-surface PD-L1/L2 expression and reduces T cell activation. Mouse melanoma tumors grow faster with Itch knockdown only in syngeneic hosts but not in immune-deficient mice. MAPK inhibitor therapy induces tumor cell-surface PD-L1 expression in murine melanoma, recapitulating the responses of clinical melanoma3, and this induction is more robust with Itch knockdown. Notably, suppression of ITCH expression first elicits a shift toward an immune-suppressive microenvironment and then accelerates resistance development. These findings collectively identify ITCH as a critical negative regulator of PD-L1 tumor cell-surface expression and provide insights into previously unexplained role of PD-L1 in adaptive resistance to therapy.

2022-03-31 | MSV000089180 | MassIVE

Gene-expression profiles of PD-L1-affected CD8+ T cells

Project description:Programmed cell death 1 ligand 1 (PD-L1) is known to suppress immune system and to be an unfavorable prognostic factor in ovarian cancer. The purpose of this study was to elucidate the function of PD-L1 in peritoneal dissemination. Tumor cell lysis by CTLs was attenuated when PD-L1 on tumor cells was overexpressed and promoted when it was silenced. PD-L1 overexpression also inhibited gathering and degranulation of CTLs. Gene expression profile of mouse CTLs caused by PD-L1-overexpressing ovarian cancer was related to human CTLs exhaustion. In mouse ovarian cancer dissemination models, depleting PD-L1 expression on tumor cells resulted in inhibited tumor growth in the peritoneal cavity and prolonged survival. Restoring immune function by inhibiting immune-suppressive factors such as PD-L1 may be a promising therapeutic strategy for peritoneal dissemination. Genome-wide transcriptional changes in OT-1 mouse CD8+ T cells that were co-incubated with OVA peptide-loaded ID8 mouse ovarian cancer cell lines. CTLs from 4 mice were devided into 2 groups, and co-incubated with PD-L1-overexpressed ID8 or PD-L1-depleted ID8.

2012-07-09 | E-GEOD-39205 | biostudies-arrayexpress

Human lung cancer TMT-labeling LC-MS

Project description:Although the paradigm of cancer treatment has changed with the recent development of drugs targeting immune checkpoints (PD-1, PD-L1, etc.), there is still a need for new targets for anticancer drugs. To discover new potential targets for immunotherapy, we compared membrane protein expression in non-small cell lung cancer cells versus normal lung cancer cells and NSCLC cell lines with low and high PD-L1 expression using mass spectrometry. As a result, it was confirmed that membrane protein, which is one of the most highly expressed proteins in NSCLC cell lines, is highly expressed in normal cells and highly expressed in cells with low PD-L1 expression.

2024-01-08 | PXD044086 | Pride

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