ABSTRACT
Regulatory T (Treg) cells that express forkhead box P3 (Foxp3) are pivotal to the maintenance of peripheral immunological tolerance [1–3]. They play a critical role in controlling autoimmunity and limiting tissue destruction and inflammation. Failure of Treg cell differentiation in humans due to loss of function mutations in FOXP3 results in fatal autoimmune lymphoproliferative disease, called immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) [1,2,4]. A similar disease (scurfy phenotype) is also seen in Foxp3 mutant mice [5–8]. Consistent with this role of Foxp3 106in mediating Treg cell phenotypic stability, it has been shown in mice that Foxp3 deficiency does not impair Treg cell development per se, but rather abrogates immunoregulatory function [6,9]. In this chapter, we define methods to study Treg cell generation, phenotype, suppressive capacities, and stability. We also describe how to expand or deplete Treg cell population as well as the different Foxp3-related mouse strains available to study Treg cell biology.
