Hydroxychloroquine suppressed endosomal TLR-induced IFNα and IL-6 release in vitro
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PBMCs were stimulated with endosomal TLR ligands in the presence of a dose range of HCQ for 24 h, and supernatants were analyzed for IRF-mediated IFNα and for NFκB-mediated IL-6 secretion. PBMCs were stimulated with different endosomal TLR ligands: poly I:C (TLR3), imiquimod (TLR7), CpG class A (TLR9), and poly I:C lyovec (RIG-I). HCQ dose-dependently inhibited endosomal TLR-induced IFNα and IL-6 secretion (Fig. HCQ dose-dependently inhibited endosomal TLR-induced IFNα and IL-6 release in vitro. PBMCs were stimulated with 50 μg/mL poly I:C (TLR3), 1 μg/mL IMQ (TLR7), 2.5 μM CpG-A (TLR9), or 1 μg/mL poly I:C/lyovec (RIG-I) for 24 h in the presence of a dose range of HCQ. IFNα and IL-6 release was measured by ELISA. The mean ± SD of the change from baseline of 6 subjects is shown. The IC