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. 2020 May 14;10(5):57. doi: 10.1038/s41408-020-0324-3

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a Malignant cells (SeAx) were cultured alone or together with nonmalignant cells (MF1850), and in the presence of vehicle (PBS) or S. aureus enterotoxin A (SEA) with and without exogenous IL-2 for 48h. pY-STAT5 was determined by flow cytometry. b Nonmalignant cells (MF1850) were cultured alone or together with malignant cells (SeAx), and in the presence of vehicle (PBS) or SEA with and without exogenous IL-2 for 48h. pY-STAT5 was determined by flow cytometry. c Malignant cells (SeAx) were treated with nontargeting siRNA control or siRNA targeting STAT5, and cultured with nonmalignant (MF1850) in the presence of SEA. FOXP3 expression was determined by qPCR. FOXP3 mRNA was normalized to that of GAPDH mRNA and it is depicted as fold change compared to nontargeting siRNA control.