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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. 2 — PI3Kγ signaling in hematopoietic cells is essential for mouse resistance to T. cruzi infection. a–c Body weight (a) and survival rate of C57BL/6 WT (n = 10) and Pik3cg^−/− (n = 10) (b) or Pik3cg^KD/KD (n = 10) (c) mice infected with 10³ trypomastigote forms of T. cruzi Y strain. d, e Blood parasitemia of WT and Pik3cg^−/− (d) or Pik3cg^KD/KD (e) mice infected with 10³ trypomastigote forms of T. cruzi Y strain. f Survival rate of chimera mice infected with 500 trypomastigote forms of T. cruzi Y strain. *P < 0.05, ***P < 0.001, and ns = no statistical significance (unpaired Student’s t-test in a, d, e and Mantel–Cox log-rank test in b, c, f). Data are representative of two (f) of three (a–e) independent experiments (mean ± s.e.m in a, d, e)