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. 2016 Aug 16;12(8):e1005782. doi: 10.1371/journal.ppat.1005782

Fig 7. HDACi decrease NK function.

Fig 7

A) NK cells treated with or without HDACi (as PBMC) for 24h (effectors) were co-cultured or not with HIV-1 LAI-infected 100nM panobinostat treated CD4 T cells (targets) and uninfected CD4 T cells (non-targets) overnight at an E:T:NT ratio of 10:1:1 (n = 4). Percent killing based on p24 reduction is shown and a Mann-Whitney U test was performed. B) NK cells were treated with 333nM vorinostat (n = 7), 20nM panobinostat (n = 8) and 10nM romidepsin (n = 7). Targets were infected CD4 T cells treated with 20nM panobinostat. A Kruskal-Wallis test with Dunn’s test for multiple comparisons was performed. C) NK cells treated with or without 333nM vorinostat, 20nM panobinostat, or 10nM romidepsin were cultured for 5h with K562 cells at a 1:1 ratio after which extracellular CD107a was measured (n = 8). A Friedman test with Dunn’s multiple comparison test was performed. D) A FATAL assay was performed using NK cells treated with or without 333nM vorinostat, 20nM panobinostat, or 10nM romidepsin (effectors) which were co-cultured with Cell Trace Violet labeled K562 cells (targets) and CFSE labeled THP1 cells (non-targets) at a 1:1:1 ratio overnight. The ratio of targets:non-targets with and without NK cells was then used to determine percent killing (n = 3).