Psoriasis skin lesions are created through chronic T-cell activation and expansion of autoreactive, skin resident αβ T helper type 17 (Th17) cell clones (Matos et al., 2017), suggesting a defect in normal tolerance mechanisms. A previous study determined that although psoriasis patients have normal numbers of circulating regulatory T (Treg) cells (CD4+CD25+Foxp3+ T cells), psoriatic Treg cells were less effective at suppressing alloreactive T cells compared with Treg cells from healthy individuals (Bovenschen et al., 2011; de Boer et al., 2007; Sugiyama et al., 2005).
