Regulatory T cell suppress cytotoxic T cells in autoimmunity and cancer by taking up IL-2.

There is limited epigenetic conservation of lineage-specific DNA elements in Treg cells, and genetic variation in Treg cell specific enhancers is associated with autoimmune disease.

The prolyl hydroxylase domain 2 regulates the Treg development and function in a hypoxia-inducible factor 2α-dependent manner.

A panel of interleukin-2 partial agonists designed to exploit distinct immune cell response thresholds enabled selective activation of regulatory T cells in vivo.

Calcium-calcineurin signaling cascade drives the acquisition of both the phenotype of the most self-reactive naive CD4 T cells and their enhanced cell-intrinsic ability to commit into induced regulatory T cells upon activation.

Foxp3 and Ikaros, two transcription factors genetically linked to autoimmune disease in humans, cooperate to establish the epigenomic and transcriptomic landscape of regulatory T cells.

Digitalized TCR repertoire-based view on antigenic specificity, plasticity, and tissue residence of regulatory T cells.

RNA processing regulates gene expression of the key transcription factor FOXP3 in T regulatory cells impacting immune tolerance and susceptibility to autoimmune disease.

The transcriptional adapter protein NCOR1 that links chromatin-modifying enzymes with gene-specific transcription factors controls naive and effector regulatory T cell states.

In localized autoimmune disease, there is autoantigen-driven expansion of both effector T cell and Treg clones that are highly persistent and are (re)circulating, and might represent interesting therapeutic targets.