Speaker: Shohei Hori, Tokyo University, Japan
Host: Ryo Morimoto, Department of Molecular Biology, MIMS
Regulatory T (Treg) cells are central guardians of immune tolerance and tissue homeostasis. This notion is firmly supported by the finding that defective Treg development and function, caused by mutations in the Foxp3 gene, lead to devastating autoimmune diseases in both mice and humans. However, the molecular mechanisms that establish the epigenetic, transcriptional, and functional identity of Treg cells remain incompletely understood. Although Foxp3 has long been regarded as the master transcription factor of Treg cells, earlier studies suggested that its role in shaping their heterogeneous epigenetic and transcriptional landscapes might be limited or indirect. Our recent findings challenge this view. Using complementary gain- and loss-of-function approaches, we demonstrate that Foxp3 plays a more fundamental and direct role than previously appreciated, integrating cell-intrinsic states and environmental contexts to drive epigenetic and transcriptional programs that define Treg cell identity and function. Acting as a master yet context-dependent regulator, Foxp3 cooperates with signal-dependent transcription factors, including BATF, to coordinate the epigenetic and transcriptional programs underlying Treg cell identity and function.
About IBSS
Integrated Biomedical Science Seminars is a broad, open seminar series within life science.