Impaired Treg-mediated immunosuppression was because of intrinsic defects in Tregs, rather than resistance of effector T cells. (A) Tregs from AA patients (n = 6) could not suppress Tresp from controls (n = 6, 7.1% ± 3.8%) to the same degree as Tregs from controls (33.9% ± 3.4%, P = .035), and Tregs from controls had more suppressive potential for Tresp from AA patients (27.4% ± 0.6%) than that of Tregs from AA patients (12.1% ± 1.6%, P = .043). (B) Tregs from AA patients had less efficiency in suppressing healthy Tcyt (7.7% ± 2.6%), but healthy Tregs could effectively inhibit its autologous Tcyt (29.8% ± 3.5%, P = .043). Likewise, it was healthy Tregs (28.1% ± 1.7%) but not for Tregs from AA patients (9.1% ± 0.4%) that exerted immunosuppressive response for Tcyt from AA patients (P = .047). * P < .05.