Fig. 2: STING agonists induce almost complete depletion of monocyte populations in PBMCs.

Human PBMCs were treated for 16 h with TLR agonists: TLR7 agonist GS-9620, TLR3 agonist poly I:C (HMW), TLR9 agonist CpG-A (ODN2216), TLR7/8 agonist Resiquimod, TLR2/7 agonist Adilipoline, and STING agonists: diaminobenzimidazole-based agonist (diABZI), 3′,3′c-di(2′F,2′d-AMP) (3′3′cdiFAA), and 2′,3′-cGAMP (2′3′cGA). Untreated cells (UT) were used as control samples. The frequency of immune populations was analyzed using multiplex immunophenotyping flow cytometry-based analyses. A, B The effect on immune subsets was analyzed as the relative fold difference in the frequency of the respective population between treated samples and UT (UT = 1, dashed lines). Individual donors are represented by different symbols. Data were analyzed with the Friedman test with the uncorrected Dunn’s test for multiple comparisons. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. A Effect on monocyte (Mo) populations (n = 5 PBMC donors): CD14+CD16- classical Mo (cMo), CD14+CD16+ intermediate Mo (iMo), CD14-CD16+ non-classical Mo (nMo). B Effect on dendritic cell (DC)-like populations (n = 5 PBMC donors): CD11c-CD123+ plasmacytoid DC (pDC)-like, CD11c+CD123+ DC-like, CD11c+CD123- conventional DC (cDC)-like cells. C Representative example (n = 1 PBMC donor) of unbiased multiparametric cluster analyses of the myeloid population of PBMCs and the effect of diABZI (a representative STING agonist) on immune subsets.