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IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia [ChIP-Seq]

ABSTRACT: IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia [ChIP-Seq]

PROVIDER: PRJNA1052131 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27202800.fastq.gz	Fastqsanger.gz
	SRR27202798.fastq.gz	Fastqsanger.gz
	SRR27202799.fastq.gz	Fastqsanger.gz

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IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia [ChIP-Seq]

Project description:Immunotherapy, including immune checkpoint blockade (ICB), has become an effective option for treating patients with cancer, especially those with solid tumors. Recently, T cell-based cellular therapies have extended the scope of immunotherapy to B-cell malignancies. Immunotherapy options for patients with acute myeloid leukemia (AML), however, are limited. To identify new immunotherapy approaches for AML, we performed CRISPR/Cas9 AML T cell co-culture screens. We determined that depletion of the transcription factor IRF2BP2 leads to enhanced T cell killing both in vitro and in vivo. Gene expression profiling and flow cytometry studies confirmed enhanced MHC-I expression upon IRF2BP2 loss. Chromatin binding analysis further revealed a regulatory axis whereby MHC-I expression is repressed by IRF2BP2 through its repression of the interferon alpha pathway. Our studies have identified the inhibition of IRF2BP2 as a potential strategy for enhancing T-cell-based therapies in patients with AML

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IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia [RNA-Seq]

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IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia

Project description:IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia

| PRJNA1052128 | ENA

IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia [RNA-Seq]

Project description:IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia [RNA-Seq]

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IRF2BP2-mediated MHC-I expression controls cytotoxic T cell responses in acute myeloid leukemia

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IRF2BP2 counteracts the ATF7/JDP2 heterodimer to prevent inflammatory overactivation in AML cells

Project description:Acute myeloid leukemia (AML) is a hematological malignancy characterized by the abnormal proliferation and accumulation of immature myeloid cells in the bone marrow. Inflammation plays a crucial role in AML progression, but excessive activation of inflammatory pathways can also trigger cell death. IRF2BP2 is a chromatin regulator that has been implicated in AML pathogenesis, although its precise role in this disease is not fully understood. In this study, we demonstrate that in AML cells IRF2BP2 interacts with the transcriptional heterodimer ATF7/JDP2, which is involved to activate inflammatory pathways in AML cells. We show that IRF2BP2 is recruited by the ATF7/JDP2 dimer to chromatin and counteracts its gene activating function. Loss of IRF2BP2 leads to the overactivation of inflammatory pathways, resulting in immediate cell death. Our findings suggest that a delicate balance of activating and repressive transcriptional mechanisms establishes a pro-oncogenic inflammatory set-up in AML cells, and that manipulation of the ATF7/JDP2-IRF2BP2 regulatory axis may offer a potential vulnerability for AML treatment. Thus, our study provides new insights into the molecular mechanisms underlying AML pathogenesis and identifies a potential therapeutic target for AML treatment.

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IRF2BP2 counteracts the ATF7/JDP2 heterodimer to prevent inflammatory overactivation in AML cells [ChIP-seq]

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