METTL16 licenses T cell expansion via m(6)A-independent translational control.

METTL16 supports CD4+ T cell activation-driven proliferation by promoting global protein synthesis and translation of Myc, independent of its methyltransferase activity.

• Why it matters: Rapid protein production is essential for T cell expansion, but how RNA-modifying enzymes function without methyltransferase activity is unclear, especially in intestinal inflammation.
• What they did: Single-cell transcriptomics showed higher METTL16 in CD4+ T cells from inflammatory bowel disease patients; T cell-specific knockout models and a catalytically inactive METTL16 mutant assessed proliferation and translation.
• The result: METTL16 loss impaired cell-cycle progression and reduced adoptive-transfer colitis induction, while the inactive mutant restored proliferation and METTL16 promoted translation initiation factor 3 complex–linked protein synthesis.

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