Invited talk 2
Prof. Shohei HORI

Laboratory of Immunology and Microbiology,
Graduate School of Pharmaceutical Sciences,
The University of Tokyo

Dr. Hori has been studying the mechanisms of immunological self-tolerance, particularly those that are mediated by Foxp3+ Treg cells. In 2003, together with Dr. Shimon Sakaguchi, he identified Foxp3 as a “master” transcription factor that controls Treg cell development and function. After establishing his own laboratory at RIKEN Research Center for Allergy and Immunology in 2004, his group continues to study the mechanisms that control the stability and adaptability of Treg cells. His group demonstrated that the vast majority of Foxp3+ T cells constitute a committed Treg cell lineage that maintains epigenetic memory of Foxp3 expression and suppressive function. However, the immune system harbors a small fraction of Foxp3+ T cells that do not possess such epigenetic memory and differentiate to helper T cells in response to perturbations from the extracellular environment. More recently, his team also uncovered a molecular mechanism that controls the ability of Treg cells to change their phenotype and adapt to various tissue and inflammatory environments. In October 2016, his laboratory moved to the Graduate School of Pharmaceutical Sciences, The University of Tokyo.

Topic:  Molecular control of Treg cell function by transcription factor Foxp3 and T cell receptor signals

Summary:  Foxp3+ regulatory T (Treg) cells are essential for the acquisition and maintenance of immunological self-tolerance and tissue homeostasis. The transcription factor Foxp3 and T cell receptor (TCR) signals represent key determinants of Treg cell differentiation and function. Treg cells require TCR signals at two distinct phases; one is for the induction and epigenetic imprinting of Foxp3 expression during thymic and extrathmic Treg cell differentiation, and the other for their effector functions and adaptation to tissue environments. In my talk, I will show that Foxp3 and TCR signals cooperate to control the phenotype and function of Treg cells. The molecular mechanisms of their interaction and its implication in self-tolerance will be discussed.