Fig. 3

E2 could upregulate HERV-E clone 4–1 mRNA expression via ER-α in CD4⁺ T cells from SLE patients. a Predicted wild-type (wt) binding sites and corresponding mutant (mut) sites of ER-α on HERV-E clone 4–1 5’LTR. b-e qRT-PCR and western-blot assays showing relative ER-α mRNA and protein expression in CD4+ cells from SLE patient with ER-α overexpression or knockdown. f Luciferase assays were performed in CD4⁺ T cells from SLE patient transfected with wt or mut luciferase reporter. Each luciferase activity was normalized to the value obtained in the cells transfected with vector. g ChIP assay was used to assess ER-α binding site at HERV-E clone 4–1 5’LTR. h Relative HERV-E clone 4–1 mRNA expression in CD4+ cells from SLE patient with ER-α overexpression compared using the paired Student’s t test. i and j Relative HERV-E clone 4–1 mRNA expression in CD4⁺ cells from SLE patient with ER-α inhibition using siRNA or AZD9496 compared using the paired Student’s t test. k and l Relative HERV-E clone 4–1 mRNA expression in CD4⁺ cells from SLE patient when ER-α siRNA or AZD9496 was used after E2 treatment compared using the paired Student’s t test. Data were represented as mean ± SD, N = 3. *P < 0.05, **P < 0.01, ***P < 0.001