2022 Volume 36 Issue 4 Pages 177-188
Although inflammatory responses to microbes by helper T (Th) cells, such as Th1, Th2, and Th17 cells, in the gut are essential for host defense against invading pathogens, aberrant effector responses can cause disruption of tissue homeostasis. Therefore, a balance between inflammatory responses and immunological tolerance is elaborately regulated by Foxp3+ regulatory (Treg) cells through several mechanisms. Patients with IPEX syndrome spontaneously develop colitis and autoimmune diseases caused by FOXP3 mutations that result in reduced suppressive activity of Foxp3+ Treg cells, which highlights the crucial role of Foxp3+ Treg cells in the maintenance of host physiology. The human intestinal tract contains a huge number of commensal bacteria. Accumulating evidence reveals that microbial components and metabolites are involved in maintenance of gut homeostasis through the induction of Foxp3+ Treg cells. Perturbations of the microbiota community, termed dysbiosis, are observed in patients with chronic inflammatory disorders, autoimmune diseases, and nervous system diseases. Therefore, further understanding of the mechanisms by which microbiota regulate the development and function of Foxp3+ Treg cells will help identify therapeutic targets and the subsequent development of therapeutic interventions in a variety of diseases.