Title REVIEW] Type 3 regulatory T cells at the interface of symbiosis
Author Joo-Hong Park1,2* and Gérard Eberl1,2*
Address 1Microenvironment and Immunity Unit, Institut Pasteur, 75724 Paris, France, 2INSERM U1224, 75724 Paris, France
Bibliography Journal of Microbiology, 56(3),163-171, 2018,
DOI 10.1007/s12275-018-7565-x
Key Words regulatory T cells, RORγt, microbiota, mucosal immunity, homeostasis
Abstract The mammalian gastrointestinal tract accommodates trillions of bacteria, many of which provide beneficial effects to the host, including protection from pathogenic microorganisms and essential metabolites. However, the intestinal immune system needs to adapt to the constantly fluctuating microbial environment at mucosal surfaces in order to maintain homeostasis. In particular, the gut microbiota induces the differentiation of effector Th17 cells and regulatory T cells (Tregs) that express RORγt, the master regulator of antimicrobial type 3 immunity. RORγt+ Tregs constitute a major population of colonic Tregs that is distinct from thymusderived Tregs and require bacterial antigens for differentiation. The balance between Th17 cells and RORγt+ Tregs, that is, the tone of the local type 3 immune response, is regulated by the vitamin A metabolite retinoic acid produced by the host. Furthermore, Th17 cells and RORγt+ Tregs regulate intestinal type 2 immune responses, explaining how bacteria block allergic reactions. Here, we review the cellular and molecular mechanisms involved in the differentiation, regulation and function of RORγt+ (type 3) Tregs, and discuss the multiple equilibria that exist between effector T cells and Tregs, as well as between different types of immune responses, which are necessary to maintain homeostasis and health.