Mirrored Transcription Factor Control of ILC3 and T Cell Differentiation Reviewed
Start here
Wang Lei's team has synthesized over a decade of research on a mirroring mechanism in which transcription factors that govern helper T cell differentiation also determine the fate of group 3 innate lymphoid cells (ILC3). RUNX3 sustains RORγt in NKp46+ ILC3, while T-bet regulates IL-17, IL-22 and MHC-II expression. On the epigenetic side, aging-linked loss of CXXC1 reduces H3K4me3 at genes in CCR6+ ILC3, and loss of UTX blocks NKp46+ ILC3 differentiation, a block that can be rescued by overexpressing TCF7. The work, presented on 14 October 2026, maps a shared regulatory logic across innate and adaptive lymphocytes. How environmental cues regulate these epigenetic switches is still unresolved.
Written by a model from the reports · updated 2 hours ago
Coverage timeline
Follow the coverage to see the different angles.
- youtube.comWang Lei Team Reviews Mirrored Transcription Factor and Epigenetic Control of ILC3 and T Cell Differentiation
Wang Lei's team presented over a decade of work on a mirroring mechanism in which transcription factors governing helper T cell differentiation also control ILC3 fate. RUNX3 sustains RORγt in NKp46+ ILC3, T-bet regulates IL-17, IL-22 and MHC-II expression, and aging-linked loss of CXXC1 reduces H3K4me3 at CCR6+ ILC3 genes, while UTX loss blocks NKp46+ differentiation, rescueable by TCF7 overexpression. How environmental cues regulate these epigenetic switches remains open.
Heat trend for this story
Heat now 9·Peak in the comparable set 10 (Oct 18 04:00)·Change over 24h in the comparable set –
The trend compares only the participants observed in full throughout, so its set can be smaller than the heat figure itself. Move the pointer or click the chart for an hour's heat; the left and right arrow keys work too.