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Dynamic IFNβ signalling underlies treatment response to immune checkpoint therapy in cancer [bulk RNA-seq]

ABSTRACT: Dynamic IFNβ signalling underlies treatment response to immune checkpoint therapy in cancer [bulk RNA-seq]

PROVIDER: PRJNA644589 | ENA |

REPOSITORIES: ENA

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Dynamic IFNβ signalling underlies treatment response to immune checkpoint therapy in cancer [bulk RNA-seq]

Project description:The on/off dynamics of IFNβ signalling underlie the therapeutic response to immune checkpoint therapy in cancer, which can be exploited to sway the clinical trajectory in favour of response

2020-12-07 | GSE153941 | GEO

Dynamic IFNβ signalling underlies treatment response to immune checkpoint therapy in cancer

Project description:Dynamic IFNβ signalling underlies treatment response to immune checkpoint therapy in cancer

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Dynamic IFNβ signalling underlies treatment response to immune checkpoint therapy in cancer [single-cell RNA-seq]

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Time-course bulk RNAseq and single-cell RNAseq of murine AB1 mesothelioma and Renca renal cancer following immune checkpoint therapy

Project description:The on/off dynamics of IFNβ signalling underlie the therapeutic response to immune checkpoint therapy in cancer in mice

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Dynamic IFNβ signalling underlies treatment response to immune checkpoint therapy in cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

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PBAF loss leads to DNA damage induced inflammatory signalling through defective G2/M checkpoint maintenance

Project description:PBRM1 is a subunit of the PBAF (SWI/SNF) chromatin remodelling complex that is mutated in approximately 40% of clear cell renal cell carcinomas (ccRCC). PBRM1 loss has been implicated in the response to immune checkpoint inhibitor (ICI) therapy in ccRCC. However, it is unclear how PBRM1 influences this. DNA damage-induced inflammatory signalling is an important factor determining ICI therapy response. This response is kept in check by the G2/M checkpoint, which prevents progression through mitosis with unrepaired damage. Here, we show that PBRM1 is required for p53-dependent maintenance of the G2/M checkpoint. In its absence, p53-dependent transcriptional upregulation of p21 is delayed, leading to defective repression of DREAM complex targets and premature entry into mitosis. Consequently, DNA damage induced inflammatory signalling pathways are activated by cytosolic DNA. Notably, p53 is infrequently mutated in ccRCC, so PBRM1 mutational status is critical to G2/M checkpoint maintenance following DNA damage in this cancer. These findings have implications for ICI therapy responses in ccRCC.

2022-10-13 | PXD028336 | Pride

IFNβ expression is restricted to a subpopulation of splenic pDCs exhibiting a specific immune modulatory transcriptome signature

Project description:Type I IFNs are critical in initiating protective antiviral immune responses and plasmacytoid DCs (pDCs) represent a major source of these cytokines. Here we show that only few pDCs are capable to produce IFNβ after virus infection or CpG stimulation. Utilizing IFNβ/YFP reporter mice, we identify these IFNβ-producing cells in the spleen as a CCR9+CD9- pDC subset exclusively localized within the T/B cell zones. IFNβ-producing pDCs exhibit a distinct transcriptome profile with higher expression of genes encoding cytokines and chemokines, facilitating T cell recruitment and activation. These distinctive characteristics of IFNβ-producing pDCs are independent of the type I IFN receptor mediated feedback loop. Furthermore, IFNβ-producing pDCs exhibit enhanced CCR7-dependent migratory properties in vitro and in a peritoneal inflammation model they effectively recruit T cells in vivo. We define “professional type I IFN-producing cells” as a distinct subset of pDCs specialized in coordinating cellular immune responses.

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Microarray data of human moDC treated with IFNβ and TNFα

Project description:Human moDC were treated with IFNβ and TNFα or the combination of both for either 1 h or 2.5 h in triplicate and profiled by gene expression microarray

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Effects of the treatment with IFNβ and GM-CSF-secreting CT2A cells to wildtype CT2A tumor microenvironment post resection

Project description:To elucidate the underlying immune responses elicited by IFNβ and GM-CSF-secreting CT2A cells to brain tumor microenvironment post resection compared to placebo group and non-IFNβ and GM-CSF-secreting CT2A cell group

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Separable functions of Tof1/Timeless in intra-S-checkpoint signalling, replisome stability and DNA topological stress

Project description:The highly conserved Tof1/Timeless proteins minimise replication stress and promote normal DNA replication. They are required to mediate the DNA replication checkpoint (DRC), the stable pausing of forks at protein fork blocks, the coupling of DNA helicase and polymerase functions during replication stress (RS) and the preferential resolution of DNA topological stress ahead of the fork. Here we demonstrate that the roles of the Saccharomyces cerevisiae Timeless protein Tof1 in DRC signalling and resolution of DNA topological stress require distinct N and C terminal regions of the protein, whereas the other functions of Tof1 are closely linked to the stable interaction between Tof1 and its constitutive binding partner Csm3/Tipin. By separating the role of Tof1 in DRC from fork stabilisation and coupling, we show that Tof1 has distinct activities in checkpoint activation and replisome stability to ensure the viable completion of DNA replication following replication stress.

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