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. 2018 Mar 29;7:49. doi: 10.1038/s41426-018-0042-0

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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 — a The endotoxin-free rHcp1 and rHcp2B could significantly inhibit phagocytosis of RAW 264.7 cells. The functions of T6SS1 and T6SS2 were deficient in ΔclpV1ΔclpV2, which could avoid the effects of other T6SS effectors. Error bars represent the standard deviations from three independent experiments, **p < 0.01. b The Vs2 region played a key role in rHcp1 and rHcp2B binding to macrophages. Endotoxin-free rHcps (25 μg) was co-incubated with RAW 264.7 cells for 4 h and washed five times with MEM