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Genetic disruption of Pdcd-1 upstream enhancer boosts T cell function and antitumor responses
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DOI：10.1016/j.imlet.2026.107171.png)
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Abstract
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• Established an upstream enhancer knockout (UpEnh KO) strain using CRISPR–Cas9 genome editing to dissect Pdcd-1 regulation in T cells. • UpEnh deletion reduced PD-1 expression across multiple T cell subsets, including thymocytes, peripheral naïve Treg, and γδ T cells, as well as tumor-infiltrating exhausted CD8+, CD4+ Tconv, Treg, and γδ T cells. • Loss of UpEnh from the Pdcd-1 locus improved CD8+ T cell exhaustion state, boosted γδ T cell activity, and promoted more robust anti-tumor responses.
Keywords:
PD-1
Upstream enhancer
CRISPR-Cas9
T cell
Antitumor immunity
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