Figure 2
In the cytotoxic group, IL-27 inhibited CTL-mediated platelet apoptosis by decreasing granzyme B expression. (A) In the cytotoxic group (n = 23), the apoptosis of platelets cultured with CTLs was significantly higher than that of platelets cultured alone (8.85% ± 2.49% vs 5.52% ± 1.58%, P < .01); however, after the addition of IL-27, the apoptosis decreased significantly (5.79% ± 1.86% vs 8.85% ± 2.49%, P < .01) and almost returned to the level of spontaneous platelet apoptosis (5.79% ± 1.86% vs 5.52% ± 1.58%, P = .19). (B) In the cytotoxic group (n = 23), a significant reduction was observed in the concentration of granzyme B in CTLs cultured with IL-27 compared with that without IL-27 (30.54 ± 7.49 pg/mL vs 56.20 ± 12.69 pg/mL, P < .01), but not in granzyme A (28.84 ± 10.03 pg/mL vs 29.91 ± 10.12 pg/mL, P = .22) or perforin (245.80 ± 53.88 pg/mL vs 249.42 ± 56.32 pg/mL, P = .54). (C) In the cytotoxic group (n = 23), the mRNA expression of granzyme B in CTLs decreased after the addition of IL-27 (0.0220 ± 0.0158 vs 0.0655 ± 0.0292, P < .01). (D) The representative dot-plots characterized the apoptosis of platelets cultured alone (8.26%), with Z-AAD-CMK (8.33%), with autologous CTLs (13.55%), or with autologous CTLs plus Z-AAD-CMK (8.39%). (E) Granzyme B inhibition analysis was performed in 9 patients of the cytotoxic group. The apoptosis of platelets cultured with CTLs were significantly higher than that of platelets cultured alone (9.38% ± 1.89% vs 5.59% ± 1.46%, P < .01); however, after the addition of granzyme B inhibitor Z-AAD-CMK, the apoptosis decreased (5.67% ± 1.41% vs 9.38% ± 1.89%, P < .01) and returned to the level of spontaneous platelet apoptosis (5.67% ± 1.41% vs 5.59% ± 1.46%, P = .55). (F) In the cytotoxic group (n = 23), the mRNA expression of T-bet in CTLs was significantly decreased after the addition of IL-27 (0.0133 ± 0.0042 vs 0.0366 ± 0.0098, P < .01), whereas Eomes was unchanged (0.0267 ± 0.0102 vs 0.0287 ± 0.0104, P = .56). *P < .01.

In the cytotoxic group, IL-27 inhibited CTL-mediated platelet apoptosis by decreasing granzyme B expression. (A) In the cytotoxic group (n = 23), the apoptosis of platelets cultured with CTLs was significantly higher than that of platelets cultured alone (8.85% ± 2.49% vs 5.52% ± 1.58%, P < .01); however, after the addition of IL-27, the apoptosis decreased significantly (5.79% ± 1.86% vs 8.85% ± 2.49%, P < .01) and almost returned to the level of spontaneous platelet apoptosis (5.79% ± 1.86% vs 5.52% ± 1.58%, P = .19). (B) In the cytotoxic group (n = 23), a significant reduction was observed in the concentration of granzyme B in CTLs cultured with IL-27 compared with that without IL-27 (30.54 ± 7.49 pg/mL vs 56.20 ± 12.69 pg/mL, P < .01), but not in granzyme A (28.84 ± 10.03 pg/mL vs 29.91 ± 10.12 pg/mL, P = .22) or perforin (245.80 ± 53.88 pg/mL vs 249.42 ± 56.32 pg/mL, P = .54). (C) In the cytotoxic group (n = 23), the mRNA expression of granzyme B in CTLs decreased after the addition of IL-27 (0.0220 ± 0.0158 vs 0.0655 ± 0.0292, P < .01). (D) The representative dot-plots characterized the apoptosis of platelets cultured alone (8.26%), with Z-AAD-CMK (8.33%), with autologous CTLs (13.55%), or with autologous CTLs plus Z-AAD-CMK (8.39%). (E) Granzyme B inhibition analysis was performed in 9 patients of the cytotoxic group. The apoptosis of platelets cultured with CTLs were significantly higher than that of platelets cultured alone (9.38% ± 1.89% vs 5.59% ± 1.46%, P < .01); however, after the addition of granzyme B inhibitor Z-AAD-CMK, the apoptosis decreased (5.67% ± 1.41% vs 9.38% ± 1.89%, P < .01) and returned to the level of spontaneous platelet apoptosis (5.67% ± 1.41% vs 5.59% ± 1.46%, P = .55). (F) In the cytotoxic group (n = 23), the mRNA expression of T-bet in CTLs was significantly decreased after the addition of IL-27 (0.0133 ± 0.0042 vs 0.0366 ± 0.0098, P < .01), whereas Eomes was unchanged (0.0267 ± 0.0102 vs 0.0287 ± 0.0104, P = .56). *P < .01.

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