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Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies II

ABSTRACT: IFNγ neutralization by the clinically approved monoclonal antibody emapalumab mitigates severe toxicity related to CAR-T therapy Emapalumab does not impair CAR.CD19 T-cell activation signaling

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE228922 | GEO | 2023/05/04

REPOSITORIES: GEO

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Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies I

Project description:IFNγ neutralization by the clinically approved monoclonal antibody emapalumab mitigates severe toxicity related to CAR-T therapy Emapalumab does not impair CAR.CD19 T-cell activation signaling

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Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies

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

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Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies

Project description:Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies

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Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies I

Project description:Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies I

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Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies II

Project description:Neutralizing IFNγ improves safety without compromising efficacy of CAR-T cell therapy in B-cell malignancies II

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UBIQUITIN LIGASE STUB1 DESTABILIZES IFNγ-RECEPTOR COMPLEX TO SUPPRESS TUMOR IFNγ SIGNALING

Project description:The cytokine IFNγ differentially impacts on tumors upon immune checkpoint blockade (ICB). Despite our understanding of downstream signaling events, less is known about 36 regulation of its receptor (IFNγ-R1). With an unbiased genome-wide CRISPR/Cas9 screen for critical regulators of IFNγ-R1 cell surface abundance, we identified STUB1 as an E3 ubiquitin ligase for IFNγ-R1 in complex with its signal-relaying kinase JAK1. STUB1 mediates ubiquitination-dependent proteasomal degradation of IFNγ-R1/JAK1 complex through IFNγ-R1K285 and JAK1K249. Conversely, STUB1 inactivation amplifies IFNγ signaling, sensitizing tumor cells to cytotoxic T cells in vitro. This was corroborated by an anticorrelation between STUB1 expression and IFNγ response in ICB-treated patients. Consistent with the context-dependent effects of IFNγ in vivo, anti-PD-1 response was increased in heterogenous tumors comprising both wildtype and STUB1-deficient cells but not full STUB1 knockout tumors. These results uncover STUB1 as a critical regulator of IFNγ-R1, and highlight the context-dependency of STUB1-regulated IFNγ signaling for ICB outcome.

2022-03-07 | PXD030580 | Pride

Chromatin accessibility in naive and primed HeLa cells upon IFNγ treatment

Project description:chromatin accessibility (ATAC-seq) experiment. HeLa cells were primed with IFNγ for 24 hours, followed by IFNγ washout. After 48h, naïve and primed cells were induced by IFNγ for 1h and 3h. Cells were harvested at indicated time points and processed for ATAC-seq.

2023-05-06 | E-MTAB-12624 | biostudies-arrayexpress

STUB1 dampens IFNγ response in tumors by destabilizing the IFNγ receptor complex

Project description:Despite its success, immune checkpoint blockade (ICB) cannot induce durable responses in most patients. This is partially attributed to reduced sensitivity to interferon gamma (IFNγ). Thus, elevating tumor IFNγ-receptor 1 (IFNγ-R1) expression to enhance IFNγ-mediated cytotoxicity is of clinical interest. Here, we demonstrate higher IFNγ-R1 expression to sensitize tumors to IFNγ-mediated killing. To unveil the largely undefined mechanisms of IFNγ-R1 expression, we performed a genome-wide CRISPR/Cas9 knockout screen for suppressors of IFNγ-R1 tumor cell surface abundance. We uncovered STUB1 as key mediator for proteasomally degrading IFNγ-R1/JAK1 complex. Conversely, STUB1 inactivation in tumor cells amplified IFNγ signaling and sensitized to cytotoxic T cells, but permitted IFNγ-induced PD-L1 expression. Rationally combining STUB1 inactivation with anti-PD-1 treatment effectively eliminated tumors in vivo. Clinically corroborating this is a STUB1 transcriptomic signature that associates with response to anti-PD-1 treatment in two patient cohorts. Thus, uncovering STUB1 as a pivotal regulator of IFNγ signaling and a synergistic target for anti-PD-1 treatment.

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STAT1 and IRF1 enrichment in naive and primed HeLa cells upon IFNγ treatment

Project description:STAT1 and IRF1 transcription factor enrichment by CUT&RUN. HeLa cells were primed with IFNγ for 24 hours, followed with IFNγ washout. After 48h, naïve and primed cells were induced by IFNγ for 1h and 3h. Cells were harvested at indicated time points and processed for CUT&RUN

2023-05-06 | E-MTAB-12625 | biostudies-arrayexpress

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