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Th17 cells and interleukin-17 increase with poor prognosis in patients with acute myeloid leukemia.

Han Y, Ye A, Bi L, Wu J, Yu K, Zhang S - Cancer Sci. (2014)

Bottom Line: Plasma levels of interleukin (IL)-17, IL-22, IL-23, IL-1β, IL-6, and transforming growth factor (TGF)-β1 were significantly increased in blood and bone marrow in AML patients compared with healthy donors.Patients with high Th17 cell frequency had poor prognosis, whereas patients with high Th1 cell frequency had prolonged survival.Combined analysis of Th1 and Th17 cell frequencies improved the ability to predict patient outcomes.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Internal Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

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Interleukin (IL)-17A and IL-22 inhibited IL-12-inducing interferon (IFN)-γ-producing cells in peripheral blood mononuclear cells (PBMCs). (a) & (b) PBMCs from healthy donors or AML patients were activated with Th1 polarizing cytokines (IL-12, 10 ng/mL; anti-CD3 antibody, 1.5 μg/mL) with or without IL-17A (10 ng/mL) and IL-22 (10 ng/mL) for 12 days. Cells were subsequently stimulated with phorbol 12-myristate13-acetate (PMA) and ionomycin in the presence of brefeldin A, stained for intercellular IFN-γ, and analyzed by flow cytometry. A representative dot plot analysis showing percentage of IFN-γ-positive cells within gated CD3+CD4+ (CD3+CD8-) population. Results are expressed as mean ± SEM representing five independent experiments from different healthy donors or AML patients. (c) PBMCs from healthy donors or AML patients were stimulated with Th1 polarizing cytokines with or without IL-17A and IL-22 for 6 days, and supernatants were determined for IFN-γ by ELISA.
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fig05: Interleukin (IL)-17A and IL-22 inhibited IL-12-inducing interferon (IFN)-γ-producing cells in peripheral blood mononuclear cells (PBMCs). (a) & (b) PBMCs from healthy donors or AML patients were activated with Th1 polarizing cytokines (IL-12, 10 ng/mL; anti-CD3 antibody, 1.5 μg/mL) with or without IL-17A (10 ng/mL) and IL-22 (10 ng/mL) for 12 days. Cells were subsequently stimulated with phorbol 12-myristate13-acetate (PMA) and ionomycin in the presence of brefeldin A, stained for intercellular IFN-γ, and analyzed by flow cytometry. A representative dot plot analysis showing percentage of IFN-γ-positive cells within gated CD3+CD4+ (CD3+CD8-) population. Results are expressed as mean ± SEM representing five independent experiments from different healthy donors or AML patients. (c) PBMCs from healthy donors or AML patients were stimulated with Th1 polarizing cytokines with or without IL-17A and IL-22 for 6 days, and supernatants were determined for IFN-γ by ELISA.

Mentions: Interleukin-17 has been reported to reduce the production of IFN-γ in PBMCs stimulated with IL-12.(27) We therefore determined whether IL-17A and IL-22, two cytokines secreted by Th17 cells,(28) affect the generation and differentiation of Th1 cells in AML. Interleukin-17A and IL-22 significantly inhibited the IL-12-induced IFN-γ-producing cells in PBMCs isolated from healthy donors or AML patients (Fig. 5a,b). Furthermore, the production of IFN-γ was reduced in the presence of combination of IL-17A and IL-22 (Fig. 5c). The findings suggest that Th17 cells-associated cytokines down-regulate Th1 cell responses in AML patients.


Th17 cells and interleukin-17 increase with poor prognosis in patients with acute myeloid leukemia.

Han Y, Ye A, Bi L, Wu J, Yu K, Zhang S - Cancer Sci. (2014)

Interleukin (IL)-17A and IL-22 inhibited IL-12-inducing interferon (IFN)-γ-producing cells in peripheral blood mononuclear cells (PBMCs). (a) & (b) PBMCs from healthy donors or AML patients were activated with Th1 polarizing cytokines (IL-12, 10 ng/mL; anti-CD3 antibody, 1.5 μg/mL) with or without IL-17A (10 ng/mL) and IL-22 (10 ng/mL) for 12 days. Cells were subsequently stimulated with phorbol 12-myristate13-acetate (PMA) and ionomycin in the presence of brefeldin A, stained for intercellular IFN-γ, and analyzed by flow cytometry. A representative dot plot analysis showing percentage of IFN-γ-positive cells within gated CD3+CD4+ (CD3+CD8-) population. Results are expressed as mean ± SEM representing five independent experiments from different healthy donors or AML patients. (c) PBMCs from healthy donors or AML patients were stimulated with Th1 polarizing cytokines with or without IL-17A and IL-22 for 6 days, and supernatants were determined for IFN-γ by ELISA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317867&req=5

fig05: Interleukin (IL)-17A and IL-22 inhibited IL-12-inducing interferon (IFN)-γ-producing cells in peripheral blood mononuclear cells (PBMCs). (a) & (b) PBMCs from healthy donors or AML patients were activated with Th1 polarizing cytokines (IL-12, 10 ng/mL; anti-CD3 antibody, 1.5 μg/mL) with or without IL-17A (10 ng/mL) and IL-22 (10 ng/mL) for 12 days. Cells were subsequently stimulated with phorbol 12-myristate13-acetate (PMA) and ionomycin in the presence of brefeldin A, stained for intercellular IFN-γ, and analyzed by flow cytometry. A representative dot plot analysis showing percentage of IFN-γ-positive cells within gated CD3+CD4+ (CD3+CD8-) population. Results are expressed as mean ± SEM representing five independent experiments from different healthy donors or AML patients. (c) PBMCs from healthy donors or AML patients were stimulated with Th1 polarizing cytokines with or without IL-17A and IL-22 for 6 days, and supernatants were determined for IFN-γ by ELISA.
Mentions: Interleukin-17 has been reported to reduce the production of IFN-γ in PBMCs stimulated with IL-12.(27) We therefore determined whether IL-17A and IL-22, two cytokines secreted by Th17 cells,(28) affect the generation and differentiation of Th1 cells in AML. Interleukin-17A and IL-22 significantly inhibited the IL-12-induced IFN-γ-producing cells in PBMCs isolated from healthy donors or AML patients (Fig. 5a,b). Furthermore, the production of IFN-γ was reduced in the presence of combination of IL-17A and IL-22 (Fig. 5c). The findings suggest that Th17 cells-associated cytokines down-regulate Th1 cell responses in AML patients.

Bottom Line: Plasma levels of interleukin (IL)-17, IL-22, IL-23, IL-1β, IL-6, and transforming growth factor (TGF)-β1 were significantly increased in blood and bone marrow in AML patients compared with healthy donors.Patients with high Th17 cell frequency had poor prognosis, whereas patients with high Th1 cell frequency had prolonged survival.Combined analysis of Th1 and Th17 cell frequencies improved the ability to predict patient outcomes.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Internal Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

Show MeSH
Related in: MedlinePlus