Chizuko Miyamoto

TL;DR: It is found that the helper T cell fate was not fixed and that mature, antigen-stimulated CD4+ T cells terminated expression of the gene encoding ThPOK and reactivated genes of the CD8 lineage, resulting in the post-thymic termination of the helpers T cell program and the functional differentiation of distinct MHC class II–restrictedCD4+ cytotoxic T lymphocytes.

TL;DR: It is shown that inefficient upregulation of ThPOK, induced by removal of the proximal enhancer from the ThPok locus, resulted in the transdifferentiation of helper lineage–specified cells into the cytotoxic T cell lineage.

TL;DR: Group 2 innate lymphoid cells (ILC2) are important mediators for allergy, but how ILC2 are regulated under chronic inflammation is still unclear and Runx transcription factors, which normally suppresses I LC2 activation at steady state, help promote ILC1 activation and type 2 cytokine production in lung allergy mouse models.

TL;DR: It is shown that silencer‐mediated alterations of chromatin structures in cytotoxic‐lineage thymocytes establish a repressive state that is epigenetically inherited in peripheral CD8+ T cells even after removal of the silencer, implying that long‐lasting TCR signals are needed to establish stable Thpok expression activity to commit to helper T‐cell fate.

TL;DR: It is shown that Runx proteins utilize different modes to repress expression of different target genes, whereas Cd4 silencing completely depends on the V WRPY motif, both VWRPY‐dependent and ‐independent mechanisms operate to repressed ThPOK gene.