Figure 3
Figure 3. Impaired Treg-mediated immunosuppression for effector T cells in AA. (A,C) Both PB- and BM-derived Tresp and Tcyt from AA patients (n = 6) showed higher proliferative ability compared with those of controls (n = 6). PB- or BM-derived Tresp and Tcyt from AA patients (n = 6) postcocultured with autologous Tregs still retained higher proliferative ability compared with that of controls (n = 6). (B,D) PB-derived Tregs from AA patients (n = 6) were less efficient in suppressing autologous Tresp and Tcyt proliferative response compared with those of controls (n = 6). BM-derived Tregs from AA patients (n = 6) also could not suppress autologous Tresp and Tcyt compared with those of controls (n = 6). The proliferation ability was calculated using absorbance (A370nm − A492nm). Percentage of inhibition was calculated using the formula: 1 − (absorbance in the presence of Tregs/absorbance in the absence of Tregs) × 100. *P < .05; **P < .001.

Impaired Treg-mediated immunosuppression for effector T cells in AA. (A,C) Both PB- and BM-derived Tresp and Tcyt from AA patients (n = 6) showed higher proliferative ability compared with those of controls (n = 6). PB- or BM-derived Tresp and Tcyt from AA patients (n = 6) postcocultured with autologous Tregs still retained higher proliferative ability compared with that of controls (n = 6). (B,D) PB-derived Tregs from AA patients (n = 6) were less efficient in suppressing autologous Tresp and Tcyt proliferative response compared with those of controls (n = 6). BM-derived Tregs from AA patients (n = 6) also could not suppress autologous Tresp and Tcyt compared with those of controls (n = 6). The proliferation ability was calculated using absorbance (A370nm − A492nm). Percentage of inhibition was calculated using the formula: 1 − (absorbance in the presence of Tregs/absorbance in the absence of Tregs) × 100. *P < .05; **P < .001.

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