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Exhausted CD8 + T cell fate is programmed by dynamic CTCF-mediated enhancer activation and invariant CTCF-imposed barriers
Journal article   Peer reviewed

Exhausted CD8 + T cell fate is programmed by dynamic CTCF-mediated enhancer activation and invariant CTCF-imposed barriers

Wei Hu, Shaoqi Zhu, Qing Chen, Vladimir P Badovinac, Weiqun Peng and Hai-Hui Xue
Nature immunology
07/06/2026
DOI: 10.1038/s41590-026-02585-5
PMID: 42409949

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Abstract

Exhausted CD8+ T (TEX) cells undergo extensive genome reorganization during differentiation, yet the drivers of this process remain elusive. Here we show that CTCF programmed CD8+ TEX cell fates through two distinct modes of action. CTCF acquired de novo binding sites and concordantly induced open chromatin in early CD8+ TEX cells responding to chronic viral infection. The dynamic CTCF binding activated enhancers and promoted chromatin looping. Consequently, genetic ablation of CTCF diminished chromatin accessibility and interaction strength, impairing CD8+ TEX cell proliferation, effector function and bioenergetic mobilization. Conversely, invariant CTCF binding acted as essential chromatin barriers, and loss of CTCF disrupted insulation and caused aberrant chromatin self-association and undue RNA polymerase II pausing, leading to excessive activation of exhaustion- and stemness-linked genes. Thus, CTCF balanced CD8+ TEX cell differentiation by gaining dynamic binding to induce cytotoxicity and sustain metabolic fitness, while its invariant binding compartmentalized exhaustion and stemness program genes to prevent their overexuberant activation.

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