Targeting ZMYND8 unleashes IL-2 signalling to override T cell exhaustion
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TL;DR - This Nature study identifies ZMYND8 as a regulator that enforces terminal exhaustion in CD8+ T cells by suppressing IL-2R–STAT5 signalling. Deleting ZMYND8 restores effector-like T cell states and substantially improves antiviral and antitumour immunity.
- ZMYND8 inhibits p300-mediated transcriptional activation of Il2ra, which encodes a component of the IL-2 receptor.
- This inhibition dampens IL-2R–STAT5 signalling and promotes terminal CD8+ T cell exhaustion.
- ZMYND8 deletion shifts exhausted T cells toward effector-like states.
- Targeting ZMYND8 could provide a strategy for strengthening immune responses against chronic infections and tumours.
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Targeting ZMYND8 unleashes IL-2 signalling to override T cell exhaustion
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TL;DR - This Nature study identifies ZMYND8 as a regulator that enforces terminal exhaustion in CD8+ T cells by suppressing IL-2R–STAT5 signalling. Deleting ZMYND8 restores effector-like T cell states and substantially improves antiviral and antitumour immunity.
- ZMYND8 inhibits p300-mediated transcriptional activation of Il2ra, which encodes a component of the IL-2 receptor.
- This inhibition dampens IL-2R–STAT5 signalling and promotes terminal CD8+ T cell exhaustion.
- ZMYND8 deletion shifts exhausted T cells toward effector-like states.
- Targeting ZMYND8 could provide a strategy for strengthening immune responses against chronic infections and tumours.