Yoshinori Naoe

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: Results indicate that Runx proteins have important roles at multiple stages of T cell development and in the homeostasis of mature T cells.

TL;DR: It is shown that loss of Runx complex function results in derepression of IL-4 in Th1 cells, and the DNaseI hypersensitivity site IV within the mouse Il4 locus plays an important role in the repression of Il4 expression in Th ones, and it is named the Il4 silencer.

TL;DR: Identification of the transcription factors network in CD4 and CD8 lineage choice provides insight into how distinct T cell subsets are developed for regulating the adaptive immune system.

TL;DR: It is shown that Treg cell-specific deficiency of Cbfbeta, a cofactor for all Runx proteins, or that of Runx1, but not Runx3, induced lymphoproliferation, autoimmune disease, and hyperproduction of IgE.