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( A ) A <t>JAK3</t> inhibitor suppressed IL-2–mediated CD318 up-regulation on CD8 T cells. PBMCs were stimulated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) and various doses of JAK3 inhibitor. Flow cytometry data shown for mock (DMSO) versus 250 pM inhibitor treatment. n = 3. ( B ) CD318 expression was not affected by STAT5 inhibitor. PBMCs stimulated with anti-CD3 for 7 days and CD8 + T cells in the presence of rhIL-2 and STAT5 inhibitor (47 μM) were evaluated by flow cytometry. n = 6–10. ( C ) STAT5 inhibitor interferes with IL-2–dependent phosphorylation of STAT5 in CD8 T cells. PBMCs were incubated with rhIL-2 (50 IU/ml) for 30 min. Phospho-STAT5 was measured in CD8 + T cells. n = 3 to 8. ( D ) Rapamycin abrogates IL-2–dependent CD318 up-regulation in CD8 T cells. PBMCs were stimulated for 7 days with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) in the presence of various doses of rapamycin. Data were evaluated by flow cytometry. n = 4. ( E ) IL-2 activates mTOR signaling. PBMCs were incubated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) for 16 hours. PBMCs were measured for phosphorylation of mTOR and S6 by flow cytometry. n = 5, n indicates biological replicates. Data are presented as the mean ± SEM. Statistical significance was assessed using a one-way ANOVA followed by multiple-comparison analysis. ** P < 0.01 and **** P < 0.0001.
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( A ) A <t>JAK3</t> inhibitor suppressed IL-2–mediated CD318 up-regulation on CD8 T cells. PBMCs were stimulated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) and various doses of JAK3 inhibitor. Flow cytometry data shown for mock (DMSO) versus 250 pM inhibitor treatment. n = 3. ( B ) CD318 expression was not affected by STAT5 inhibitor. PBMCs stimulated with anti-CD3 for 7 days and CD8 + T cells in the presence of rhIL-2 and STAT5 inhibitor (47 μM) were evaluated by flow cytometry. n = 6–10. ( C ) STAT5 inhibitor interferes with IL-2–dependent phosphorylation of STAT5 in CD8 T cells. PBMCs were incubated with rhIL-2 (50 IU/ml) for 30 min. Phospho-STAT5 was measured in CD8 + T cells. n = 3 to 8. ( D ) Rapamycin abrogates IL-2–dependent CD318 up-regulation in CD8 T cells. PBMCs were stimulated for 7 days with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) in the presence of various doses of rapamycin. Data were evaluated by flow cytometry. n = 4. ( E ) IL-2 activates mTOR signaling. PBMCs were incubated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) for 16 hours. PBMCs were measured for phosphorylation of mTOR and S6 by flow cytometry. n = 5, n indicates biological replicates. Data are presented as the mean ± SEM. Statistical significance was assessed using a one-way ANOVA followed by multiple-comparison analysis. ** P < 0.01 and **** P < 0.0001.
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( A ) A <t>JAK3</t> inhibitor suppressed IL-2–mediated CD318 up-regulation on CD8 T cells. PBMCs were stimulated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) and various doses of JAK3 inhibitor. Flow cytometry data shown for mock (DMSO) versus 250 pM inhibitor treatment. n = 3. ( B ) CD318 expression was not affected by STAT5 inhibitor. PBMCs stimulated with anti-CD3 for 7 days and CD8 + T cells in the presence of rhIL-2 and STAT5 inhibitor (47 μM) were evaluated by flow cytometry. n = 6–10. ( C ) STAT5 inhibitor interferes with IL-2–dependent phosphorylation of STAT5 in CD8 T cells. PBMCs were incubated with rhIL-2 (50 IU/ml) for 30 min. Phospho-STAT5 was measured in CD8 + T cells. n = 3 to 8. ( D ) Rapamycin abrogates IL-2–dependent CD318 up-regulation in CD8 T cells. PBMCs were stimulated for 7 days with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) in the presence of various doses of rapamycin. Data were evaluated by flow cytometry. n = 4. ( E ) IL-2 activates mTOR signaling. PBMCs were incubated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) for 16 hours. PBMCs were measured for phosphorylation of mTOR and S6 by flow cytometry. n = 5, n indicates biological replicates. Data are presented as the mean ± SEM. Statistical significance was assessed using a one-way ANOVA followed by multiple-comparison analysis. ** P < 0.01 and **** P < 0.0001.
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( A ) A <t>JAK3</t> inhibitor suppressed IL-2–mediated CD318 up-regulation on CD8 T cells. PBMCs were stimulated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) and various doses of JAK3 inhibitor. Flow cytometry data shown for mock (DMSO) versus 250 pM inhibitor treatment. n = 3. ( B ) CD318 expression was not affected by STAT5 inhibitor. PBMCs stimulated with anti-CD3 for 7 days and CD8 + T cells in the presence of rhIL-2 and STAT5 inhibitor (47 μM) were evaluated by flow cytometry. n = 6–10. ( C ) STAT5 inhibitor interferes with IL-2–dependent phosphorylation of STAT5 in CD8 T cells. PBMCs were incubated with rhIL-2 (50 IU/ml) for 30 min. Phospho-STAT5 was measured in CD8 + T cells. n = 3 to 8. ( D ) Rapamycin abrogates IL-2–dependent CD318 up-regulation in CD8 T cells. PBMCs were stimulated for 7 days with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) in the presence of various doses of rapamycin. Data were evaluated by flow cytometry. n = 4. ( E ) IL-2 activates mTOR signaling. PBMCs were incubated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) for 16 hours. PBMCs were measured for phosphorylation of mTOR and S6 by flow cytometry. n = 5, n indicates biological replicates. Data are presented as the mean ± SEM. Statistical significance was assessed using a one-way ANOVA followed by multiple-comparison analysis. ** P < 0.01 and **** P < 0.0001.
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Fig. 8. PGG decreased the expression of <t>JAK1/JAK3-STAT3,</t> CSC-, EMT-, and anti-apoptosis- proteins in tumor lumps. (A) Expression levels and quantitative assessment of the JAK1, JAK3, t-STAT3, p-STAT3, and Bcl-2 proteins in HCT116/5-FU tumor lumps. (B) Expression levels and quantitative assessment of the CD133, CD44, and LGR5 proteins in HCT116/5-FU tumor lumps. (C) Expression levels and quantitative assessment of N-cadherin and vimentin proteins in HCT116/5-FU tumor lumps. (PGG treatment groups vs control group: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, and PGG treatment groups vs 5-FU treatment group: #p < 0.05).
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Fig. 8. PGG decreased the expression of <t>JAK1/JAK3-STAT3,</t> CSC-, EMT-, and anti-apoptosis- proteins in tumor lumps. (A) Expression levels and quantitative assessment of the JAK1, JAK3, t-STAT3, p-STAT3, and Bcl-2 proteins in HCT116/5-FU tumor lumps. (B) Expression levels and quantitative assessment of the CD133, CD44, and LGR5 proteins in HCT116/5-FU tumor lumps. (C) Expression levels and quantitative assessment of N-cadherin and vimentin proteins in HCT116/5-FU tumor lumps. (PGG treatment groups vs control group: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, and PGG treatment groups vs 5-FU treatment group: #p < 0.05).
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Image Search Results


( A ) A JAK3 inhibitor suppressed IL-2–mediated CD318 up-regulation on CD8 T cells. PBMCs were stimulated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) and various doses of JAK3 inhibitor. Flow cytometry data shown for mock (DMSO) versus 250 pM inhibitor treatment. n = 3. ( B ) CD318 expression was not affected by STAT5 inhibitor. PBMCs stimulated with anti-CD3 for 7 days and CD8 + T cells in the presence of rhIL-2 and STAT5 inhibitor (47 μM) were evaluated by flow cytometry. n = 6–10. ( C ) STAT5 inhibitor interferes with IL-2–dependent phosphorylation of STAT5 in CD8 T cells. PBMCs were incubated with rhIL-2 (50 IU/ml) for 30 min. Phospho-STAT5 was measured in CD8 + T cells. n = 3 to 8. ( D ) Rapamycin abrogates IL-2–dependent CD318 up-regulation in CD8 T cells. PBMCs were stimulated for 7 days with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) in the presence of various doses of rapamycin. Data were evaluated by flow cytometry. n = 4. ( E ) IL-2 activates mTOR signaling. PBMCs were incubated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) for 16 hours. PBMCs were measured for phosphorylation of mTOR and S6 by flow cytometry. n = 5, n indicates biological replicates. Data are presented as the mean ± SEM. Statistical significance was assessed using a one-way ANOVA followed by multiple-comparison analysis. ** P < 0.01 and **** P < 0.0001.

Journal: Science Advances

Article Title: CD318 expression defines a novel subset of human CD8 + regulatory T cells

doi: 10.1126/sciadv.adz4203

Figure Lengend Snippet: ( A ) A JAK3 inhibitor suppressed IL-2–mediated CD318 up-regulation on CD8 T cells. PBMCs were stimulated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) and various doses of JAK3 inhibitor. Flow cytometry data shown for mock (DMSO) versus 250 pM inhibitor treatment. n = 3. ( B ) CD318 expression was not affected by STAT5 inhibitor. PBMCs stimulated with anti-CD3 for 7 days and CD8 + T cells in the presence of rhIL-2 and STAT5 inhibitor (47 μM) were evaluated by flow cytometry. n = 6–10. ( C ) STAT5 inhibitor interferes with IL-2–dependent phosphorylation of STAT5 in CD8 T cells. PBMCs were incubated with rhIL-2 (50 IU/ml) for 30 min. Phospho-STAT5 was measured in CD8 + T cells. n = 3 to 8. ( D ) Rapamycin abrogates IL-2–dependent CD318 up-regulation in CD8 T cells. PBMCs were stimulated for 7 days with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) in the presence of various doses of rapamycin. Data were evaluated by flow cytometry. n = 4. ( E ) IL-2 activates mTOR signaling. PBMCs were incubated with anti-CD3 (1 μg/ml) + rhIL-2 (50 IU/ml) for 16 hours. PBMCs were measured for phosphorylation of mTOR and S6 by flow cytometry. n = 5, n indicates biological replicates. Data are presented as the mean ± SEM. Statistical significance was assessed using a one-way ANOVA followed by multiple-comparison analysis. ** P < 0.01 and **** P < 0.0001.

Article Snippet: To test CD318 expression, anti-CD3 + IL-2–stimulated PBMCs were treated with various doses of JAK3 inhibitor (FM-381; Selleckchem, catalog no. S8541) or 47 μM of STAT5 inhibitor.

Techniques: Flow Cytometry, Expressing, Phospho-proteomics, Incubation, Comparison

Fig. 8. PGG decreased the expression of JAK1/JAK3-STAT3, CSC-, EMT-, and anti-apoptosis- proteins in tumor lumps. (A) Expression levels and quantitative assessment of the JAK1, JAK3, t-STAT3, p-STAT3, and Bcl-2 proteins in HCT116/5-FU tumor lumps. (B) Expression levels and quantitative assessment of the CD133, CD44, and LGR5 proteins in HCT116/5-FU tumor lumps. (C) Expression levels and quantitative assessment of N-cadherin and vimentin proteins in HCT116/5-FU tumor lumps. (PGG treatment groups vs control group: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, and PGG treatment groups vs 5-FU treatment group: #p < 0.05).

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Pentagalloyl glucose targets the JAK1/JAK3-STAT3 pathway to inhibit cancer stem cells and epithelial-mesenchymal transition in 5-fluorouracil-resistant colorectal cancer.

doi: 10.1016/j.phymed.2025.156773

Figure Lengend Snippet: Fig. 8. PGG decreased the expression of JAK1/JAK3-STAT3, CSC-, EMT-, and anti-apoptosis- proteins in tumor lumps. (A) Expression levels and quantitative assessment of the JAK1, JAK3, t-STAT3, p-STAT3, and Bcl-2 proteins in HCT116/5-FU tumor lumps. (B) Expression levels and quantitative assessment of the CD133, CD44, and LGR5 proteins in HCT116/5-FU tumor lumps. (C) Expression levels and quantitative assessment of N-cadherin and vimentin proteins in HCT116/5-FU tumor lumps. (PGG treatment groups vs control group: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, and PGG treatment groups vs 5-FU treatment group: #p < 0.05).

Article Snippet: 5-FU, Janus kinase 1 (JAK1) inhibitors, and Janus kinase 3 (JAK3) inhibitors were purchased from MedChemExpress (New Jersey, USA).

Techniques: Expressing, Control