Dp2-induced autoantigen/autoantibody production from patients with systemic lupus erythematosus is not affected by AhR agonist

Systemic Lupus Erythematosus (SLE) is a multifactorial systemic autoimmune disorder that can produce numerous abnormalities in cellular and humoral immune responses, including abnormal autoantigen and autoantibody production by dysregulated B cells. There are many known ligands of the AhR (aryl hydrocarbon receptor) in air pollutants, such as 6-formylindolo[3,2-b] Carbazole (FICZ) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). This study investigated the effect of FICZ/TCDD on the autoantigen/autoantibody and inflammatory cytokine production of B cells in Dp-allergic SLE. Dp2-induced autoantigen/autoantibody from B cell lines and PBMC derived from Dp-allergic SLE were used to evaluate the effects of FICZ/TCDD. Autoantigen/autoantibody and inflammatory cytokines were measured after cells were stimulated with FICZ/TCDD in conjuction with Dp2. The results showed that both FICZ/TCDD can activate AhR expression and induce the mRNA expression of IL-8. There were no effects on the production of IFN- α , IL-6, or autoantigen/autoantibody, except enolase-1. In the presence of Dp2 there were no augmentation effects of FICZ/TCDD on the expression of AhR or any of the autoantigens/autoantibodies from B cell lines. Although Dp2 could induce IL-8 production from PBMC derived from Dp-allergic SLE and non-SLE patients, there were no differences between the two groups and FICZ also showed no augmentation effects on IL-8 production. In conclusion, although FICZ/TCDD can induce AhR expression and IL-8 production from B cells derived from Dp-allergic SLE. There were no augmentation effects on Dp2-induced autoantigen/autoantibody or inflammatory cytokine production by FICZ/TCDD. In the presence of Dp2, FICZ had no augmentation effect on IL-8 production from PBMC derived from patients with Dp-allergic SLE.