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. 2018 Apr 17;9:1513. doi: 10.1038/s41467-018-03986-3

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© The Author(s) 2018

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. 6 — PI3Kγ controls the heart parasitism after infection with T. cruzi. a Representative images from H&E staining of heart tissue from WT (n = 6) and Pik3cg^−/− (n = 6) mice 18 days post infection with T. cruzi Y strain. Black arrows indicate amastigote nests of the parasite. Scale bars = 20 µm. b, c Quantitative PCR analysis of T. cruzi DNA isolated from Pik3cg^−/− (b) and Pik3cg^KD/KD (c) mice 18 days post infection with T. cruzi Y strain. d Survival rate of Pik3cg^−/− mice infected with 10³ trypomastigote forms of T. cruzi Y strain and treated with 100 mg Kg⁻ of benznidazole (BNZ) (n = 8) or vehicle (n = 6). *P < 0.05, by unpaired Student’s t-test, relative to WT mice (a–c). *P < 0.05 and ***P < 0.001 (unpaired Student’s t-test in a–c and Mantel–Cox log-rank test in d). Data are from one experiment (d) or representative of two (c) or three (a, b) independent experiments (mean ± s.e.m in a–c)