Abstract
Forkhead box protein P3
(FOXP3
) regulatory T cells (T
cells) play a key role in maintaining tolerance and immune homeostasis. Here, we report that a T cell-specific deletion of the transcription factor MAZR (also known as PATZ1) leads to an increased frequency of T
cells, while enforced MAZR expression impairs T
cell differentiation. Further, MAZR expression levels are progressively downregulated during thymic T
cell development and during in-vitro-induced human T
cell differentiation, suggesting that MAZR protein levels are critical for controlling T
cell development. However, MAZR-deficient T
cells show only minor transcriptional changes ex vivo, indicating that MAZR is not essential for establishing the transcriptional program of peripheral T
cells. Finally, the loss of MAZR reduces the clinical score in dextran-sodium sulfate (DSS)-induced colitis, suggesting that MAZR activity in T cells controls the extent of intestinal inflammation. Together, these data indicate that MAZR is part of a T
cell-intrinsic transcriptional network that modulates T
cell development.