NSD2 controls CD8+ T cell fate through the H3K36me2-Zbtb20 axis
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A study published in Science Advances on October 24, 2026 shows that the histone methyltransferase NSD2 governs CD8+ T cell differentiation and fate during acute viral infection via the H3K36me2-Zbtb20 axis. Loss of NSD2 boosts the early expansion of activated CD8+ T cells but severely undermines their survival fitness during the contraction phase, collapsing the antigen-specific T cell pool and restricting long-term memory formation. In tumors, NSD2 deficiency also increases the proportion of resident memory T cells, which display a dysfunctional phenotype. The work identifies NSD2-dependent chromatin methylation as a determinant of whether CD8+ T cells become durable memory cells or fail to persist.
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- Sci AdvHistone methyltransferase NSD2 shapes CD8+ T cell fates through the H3K36me2-Zbtb20 axis.
The histone methyltransferase NSD2 controls CD8+ T cell differentiation and fate during acute viral infection through the H3K36me2-Zbtb20 axis. NSD2 loss enhances early expansion of activated CD8+ T cells but severely impairs survival fitness during the contraction phase, causing disproportionate collapse of the antigen-specific pool and limiting long-term memory formation. In tumors, NSD2 loss also raises the proportion of resident memory T cells, which show a dysfunctional phenotype.
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