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. 2018 Nov 7;8:16471. doi: 10.1038/s41598-018-34576-4

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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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Vδ1⁺ cells in HIV controllers display an activated, effector-like phenotype. PBMCs were characterized by flow cytometry and the phenotypes of viable CD3⁺Vδ1⁺ cells were assessed. (a) Representative flow plots from an HIV-uninfected subject (Neg) and an elite controller (EC). The numbers in each quadrant represent the percentage of CD3⁺Vδ1⁺ cells. (b–d) Summary data of median percentages of Vδ1⁺ cells that are CD45RA⁺CD27⁺ (b), CD45RA⁺CD27⁻ (c), or HLA-DR⁺CD38⁺ (d) for Neg (n = 17), EC (n = 15), CT (n = 13), VC (n = 4), and CU (n = 11) subjects. The medians of the cohorts were significantly different for all three (b-d) summary graphs (p < 0.0001) as assessed by the Kruskal-Wallis test. Dunn’s multiple comparison tests were used to assess differences between HIV⁻ and HIV⁺ groups. *p < 0.05; **p < 0.01; ***p < 0.001.