About the book
CD4+FOXP3+ regulatory T cells (Treg) have an indispensable role in maintaining immune homeostasis and immune tolerance. They control unwanted immune responses that are involved in the regulation of immune tolerance to self as well as to foreign antigens. Loss-of-function mutation in FOXP3 locus, a gene encoding Treg lineage transcription factor FOXP3, leads to multiorgan autoimmune associated disease including diabetes, thyroiditis, eczema, hyper-IgE syndrome, and cytokine storm. However, FOXP3+ Treg might become unstable especially under certain inflammatory conditions, and might transform into proinflammatory cytokine-producing cells. The issue of heterogeneity and instability of Treg has caused considerable debate in the field and has important implications for Treg-based immunotherapy. Modulation of Treg is proposed as a means of treating autoimmunity and preventing organ transplant rejection. For optimizing these Treg-based therapies, it is vital to get a better understanding of Treg expansion, migration, and suppressive function. Besides, it is essential to consider the metabolic profiles of Treg throughout these capacities. A full understanding of Treg metabolic profile throughout proliferation, migration, and suppressive function, as well as how Treg metabolism could be exploited for tolerance-inducing therapies for autoimmune diseases are a few popular research topics at the current moment.