1678-Targeting ZMYND8 Overrides T Cell Exhaustion
The research investigates the epigenetic and molecular mechanisms that drive CD8+ T cell exhaustion during chronic viral infections and cancer, identifying ZMYND8 as a critical chromatin reader that represses IL-2R–STAT5 signaling. Through in vivo single-cell CRISPR screens, the study demonstrates that ZMYND8 suppresses effector-like states and promotes terminal exhaustion by binding to active enhancer regions of the Il2ra gene and suppressing p300 histone acetyltransferase activity. Consequently, deleting or targeting ZMYND8 unleashes effector-like cell differentiation—particularly the…
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