Yohko Kitagawa

TL;DR: Understanding how epigenetic alterations and Foxp3 expression coordinately control Treg-cell-specific gene regulation will enable better control of immune responses by targeting the generation and maintenance of Treg cells.

TL;DR: Results suggest that Satb1-dependent Treg-SE activation is crucial for Treg cell lineage specification in the thymus and that its perturbation is causative of autoimmune and other immunological diseases.

TL;DR: It is suggested that, similar to Tfh cells, Tfr cells follow a differentiation pathway generating a mature GC-localized subpopulation, CD25− Tfr Cells, which is preferentially located in the GC and can be clearly differentiated from CD25+ non–GC-Tfr, TfH, and effector Treg cells by the expression of a wide range of molecules.

TL;DR: Recent genome-wide studies reveal that Foxp3+ natural Treg cells possess a number of unique transcriptional and epigenetic features, which appear to be acquired along the course of Treg cell development and maintained throughout their lifespan.

TL;DR: The results indicate that CDK8/19 is physiologically repressing Foxp3 expression in activated conventional T cells and that its pharmacological inhibition enables conversion of antigen-specific effector/memory T cells into Foxp 3+ Treg cells for the treatment of various immunological diseases.