Abstract
Regulatory T (Treg) cells play a vital role in the prevention of autoimmunity and the maintenance of self-tolerance, but these cells also have an active role in inhibiting immune responses during viral, bacterial, and parasitic infections. Although excessive Treg activity can lead to immunodeficiency, chronic infection, and cancer, too little Treg activity results in autoimmunity and immunopathology and impairs the quality of pathogen-specific responses. Recent studies have helped define the homeostatic mechanisms that support the diverse pool of peripheral Treg cells under steady-state conditions and delineate how the abundance and function of Treg cells changes during inflammation. These findings are highly relevant for developing effective strategies to manipulate Treg cell activity to promote allograft tolerance and treat autoimmunity, chronic infection, and cancer.