Figure 3

Vδ1⁺ cells in HIV controllers produce inflammatory cytokines. PBMCs were stimulated with PMA/ionomycin for 6 hours and cytokine production was measured by intracellular cytokine staining. Viable CD3⁺Vδ1⁺ cells were analyzed for production of IFNγ, TNFα, MIP1β, and IL-17A. (a) Representative flow plots from an HIV-uninfected subject (Neg) and an elite controller (EC) showing percentages of Vδ1⁺ cells expressing IFNγ and TNFα. (b) Summary data showing the median percentage of viable CD3⁺ cells that are IFNγ⁺TNFα⁺MIP1β⁺ Vδ1⁺ for Neg (n = 9), EC (n = 14), CT (n = 11), and CU (n = 7) subjects. The medians were significantly different (p = 0.0008) as assessed by the Kruskal-Wallis test. Dunn’s multiple comparison tests were used to assess differences between HIV⁻ and HIV⁺ groups. (c) The median distribution of Vδ1⁺ cells producing the indicated number of cytokines in each cohort. The distributions in HIV-infected cohorts were significantly different than that of HIV-uninfected subjects as assessed by the permutation analysis in SPICE (n = 10,000 iterations). *p < 0.05; **p < 0.01; ***p < 0.001. (d) Spearman’s rank correlation between the frequency of pro-inflammatory IFNγ⁺TNFα⁺MIP1β⁺ Vδ1⁺ cells of total CD3⁺ cells and the frequency of activated (HLA-DR⁺CD38⁺) CD8⁺ T cells out of total CD8⁺ T cells; Spearman’s ρ = 0.7107, p < 0.0001; the same subjects as in c, without CT (30 total subjects).