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Figure 1 WBC count (A), platelet count (B), MPV (C), platelet activation rate (D) and TGF-β1concentration (E) in the PF of women with endometriosis and.

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Presentation on theme: "Figure 1 WBC count (A), platelet count (B), MPV (C), platelet activation rate (D) and TGF-β1concentration (E) in the PF of women with endometriosis and."— Presentation transcript:

1 Figure 1 WBC count (A), platelet count (B), MPV (C), platelet activation rate (D) and TGF-β1concentration (E) in the PF of women with endometriosis and controls. Data are represented as mean ± SD. Boxplot of WBC count (F) and platelet activation rate (G) by the revised American Society for Reproductive Medicine Classification of endometriosis (rASRM) stage. The numbers shown are Spearman's correlation coefficients. *P < 0.05; **P < 0.01; ***P < From: Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis Hum Reprod. 2016;31(7): doi: /humrep/dew057 Hum Reprod | © The Author Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please

2 Figure 2 Scatter plots showing the relationship, in the PF, (A) between the TGF-β1 concentration and platelet activation rate; (B) between the TGF-β1 concentration and the WBC count; (C) between the WBC count and the platelet count; (D) between the platelet activation rate and the WBC count. In all figures, the dashed line represents the linear regression line and the number, the correlation coefficient, which is followed by the sign of statistical significance level: **P < 0.01; ***P < From: Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis Hum Reprod. 2016;31(7): doi: /humrep/dew057 Hum Reprod | © The Author Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please

3 Figure 3 Representative flow cytometric data showing (A) CD3–CD56+, CD3–CD56<sup>bright</sup> and CD3–CD56<sup>dim</sup> gatings were set to identify NK cells from the PF. (B) The percentage of NKG2D-positive NK cells in CD3–CD56+, CD3–CD56<sup>bright</sup> and CD3–CD56<sup>dim</sup> NK cells in PF of controls and patients with endometriosis were shown in dot plots. The expression of NKG2D+ NK cells among total CD56+, CD56<sup>bright</sup> and CD56<sup>dim</sup>NK cells are shown. The expression of NKG2D in total CD56<sup>+</sup>, CD56<sup>bright</sup>, CD56<sup>dim</sup>NK cells of endometriosis were significantly higher than that in controls. The percentage of NKG2D-expressing NK cells among total CD56+ (C), CD56<sup>bright</sup> (D) and CD56<sup>dim</sup> (E) NK cells. ***P < 0.001; data are represented in mean ± SD. Control, PF from controls; EM, PF from women with endometriosis. FSC-H, forward scatter-height; SSC-H, side scatter-height. From: Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis Hum Reprod. 2016;31(7): doi: /humrep/dew057 Hum Reprod | © The Author Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please

4 Figure 4 Boxplots showing the percentage ofNKG2D-expressing NK cells among total CD56+ (A) and CD56<sup>dim</sup> (B) in women with rASRM Stages II and III/IV endometriosis. Scatter plots showing the relationship, in the PF, (A) between the percentage of NKG2D+NK cells in total CD56+NK cells and the platelet activation rate; (B) between the percentage of NKG2D+NK cells in CD56<sup>bright</sup> NK cells and the platelet activation rate; (C) between the percentage of NKG2D+NK cells in CD56<sup>dim</sup> NK cells and the platelet activation rate; (D) between the percentage of NKG2D+NK cells in CD56<sup>dim</sup> NK cells and the TGF-β1 concentration. In all figures, the dashed line represents the linear regression line and the number, the correlation coefficient, which is followed by the sign of statistical significance level: *P < 0.05; **P < 0.01; ***P < From: Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis Hum Reprod. 2016;31(7): doi: /humrep/dew057 Hum Reprod | © The Author Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please

5 Figure 5 (A) NK cell cytotoxicity was significantly decreased after co-culture with the PF collected controls and endometriosis patients, when compared with those co-cultured with RPMI % PBS only. (B) Effect of TGF-β1 blockade on cytotoxicity of NK cell cultured with PF collected from controls. Untreated: RPMI % PBS only; non-immune IgG: treatment with 5 μg/ml isotype-matched non-immune IgG antibody; TGF-β1 blockade: treatment with 5 μg/ml anti-TGF-β1 antibody. (C) Effect of TGF-β1 blockade on cytotoxicity of NK cell cultured with PF collected from patients with endometriosis. Untreated: RPMI % PBS only; non-immune IgG: treatment with 5 μg/ml isotype-matched non-immune IgG antibody; TGF-β1 blockade: treatment with 5 μg/ml anti-TGF-β1 antibody. NK cell cytotoxicity was significantly restored after TGF-β1 blockade. *P < 0.05; **P < 0.01; ***P < 0.001, all compared with the ‘untreated’ group; <sup>##</sup>P < 0.01; <sup>###</sup>P < 0.001, all compared with the non-immune IgG group; NS, statistically not significant, i.e. P > 0.05; NKC, NK cell. Data are represented in mean ± SD. (D) Percentage of early apoptotic NK cells after indicated treatment. (E) Percentage of late apoptotic NK cells after indicated treatment. (F) Percentage of viable NK cells after indicated treatment. +ve CTL, positive control (treated with cyclosporin A); Untreated, treated with PBS; CTL PF, treated with PF from women without endometriosis; ENDO PF, treated with PF from women with endometriosis. NS, statistically not significant, when compared with untreated NK cells. From: Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis Hum Reprod. 2016;31(7): doi: /humrep/dew057 Hum Reprod | © The Author Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please

6 Figure 6 (A) Effect of treatment of PF collected from women with endometriosis on the expression of NKG2D on freshly isolated NK cells, when compared with those from controls (n≥ 8 in each experiment). Data are represented in mean ± SD. (B) Effect of TGF-β1 blockade on the NKG2D expression of NK cells cultured with PF collected from patients with endometriosis. Non-immune IgG: treated with 5 μg/ml isotype-matched non-immune IgG antibody; Anti-TGF-β1: treated with 5 μg/ml anti-TGF-β1 antibody. *P < 0.05, compared with the control or non-immune IgG control. From: Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis Hum Reprod. 2016;31(7): doi: /humrep/dew057 Hum Reprod | © The Author Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please

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