ArticleJournal for immunotherapy of cancer2025
STS2 deficiency revives CD8
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- CRISPR-screen informed engineered T cell therapies.Frontiers in immunology · 2026Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundT-cell exhaustion is a major barrier to effective antitumor immunity and limits the efficacy of cancer immunotherapies. This study investigates the role of suppressor of T-cell signaling 2 (STS2, also known as UBASH3A) in regulating CD8
methodsWe used genetic ablation of STS2 in mouse models to assess tumor control and responses to anti-programmed cell death protein 1 (PD-1) checkpoint blockade therapy. CD8
resultsSTS2 expression progressively increased with T-cell exhaustion. Genetic deletion of STS2 enhanced tumor control and improved responses to anti-PD-1 therapy. STS2-deficient CD8
conclusionsOur findings establish STS2 as a multifaceted regulator of T-cell exhaustion and highlight its potential as a therapeutic target for enhancing antitumor immunity and improving cancer immunotherapy outcomes.
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Registered trials
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