Skip to main content
. 2021 Oct 21;17(10):e1010014. doi: 10.1371/journal.ppat.1010014

Fig 6. Inhibition of UTX by GSK-J4 promotes the silencing of HIV-1 in Th17 primary cells and elevates HIV-1 DNA methylation.

Fig 6

(A) Schematic of experimental design. (B) Relative levels of H3K27me3 compared to histone H3 levels quantified from Western blot on treated Th17 cells from 4 donors at Day 4. One-tailed, paired t-test, * p<0.05. (C) Silencing kinetics of HIV-1 in Th17 cells from 4 different donors in the presence of 0 μM (vehicle) or 1 μM of GSK-J4. Error bars: SEM of at least 3 separate biological replicates. Two-way ANOVA, Bonferroni posttests, * p<0.05 ** p<0.01. (D) MeDIP measuring the levels of methylated cytosine of HIV-1 at Day 4. Error bars: SEM of 4 different donors. One-tailed, paired t-test, n = 4, * p<0.05. (E) GSK-J4 inhibits the reactivation of latent HIV-1 by SAHA & IL15 or TCR stimulation in Th17 primary cells. Cells were pretreated for 24 hours with GSK-J4, then further stimulated overnight with SAHA & IL15 or Human T-Activator CD3/CD28 Dynabeads with the ratio of 25 μl of beads per 1 million cells. Quantification of HIV-1 reactivation under the indicated conditions. Note that only viable cells were chosen for HIV-1 reactivation measurement. Error bars: SEM of more than 3 separate replicates. One-way ANOVA, Bonferroni posttests n >3.