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ATF7ip inhibits the tumor immune response by promoting terminal CD8+ T cell Exhaustion III

GSE305486 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/04/23 Platform GPL34328
Summary
CD8+ T cell exhaustion limits the immune response to tumors because of ineffective T cell effector functions. Thus, therapies that inhibit T-cell exhaustion are critical for optimizing cancer treatment. Recent studies have implicated epigenetic proteins in T-cell exhaustion. Here, we identified activating transcription factor 7 interacting protein (ATF7ip) as an epigenetic protein critical for inducing T cell exhaustion. Loss of Atf7ip in CD8+ T cells results in decreased terminal exhaustion and increased numbers of progenitor-exhausted cells in both chronic viral infections and cancer. Owing to decreased exhaustion, Atf7ip-deficiency in CD8+ T cells leads to an enhanced immune response to tumors. Mechanistically, ATF7ip functions to stimulate the deposition of repressive H3K9me3 at critical immune-effector gene loci, such as Il7r and Il2 leading to enhanced exhaustion. Our data suggest that ATF7ip may be a rational target for deletion in adoptive T-cell therapies to reduce CD8+ T-cell exhaustion.
Published in
ATF7ip Inhibits the Tumor Immune Response by Promoting Terminal CD8+ T-cell Exhaustion
Kashyap S, Sin JH, Guldberg SM et al. · Cancer immunology research 2026 · PMID 41973040 · doi:10.1158/2326-6066.CIR-25-0816
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Also filed as BioProject PRJNA1306076 and SRA study SRP608966. Searching any of these in the dataset finder brings you back here.

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