Fig. 1

MiR-223 is a key factor of SLE in MRL/lpr mice. (A) MiR-223 was upregulated in neutrophils of MRL/lpr mice (miR-223) (n = 12) compared to BALB/c mice (n = 12), and miR-223 expression decreased significantly in MRL/lpr mice after treatment with 20nmol (n = 6) and 40nmol (n = 6) miR-223 inhibitor. MRL/lpr mice in miR-223 knockdown group showed decreased levels of proteinuria (B) and dsDNA antibody (C) and increased level of C3 (D). HE staining (E) showed prominent glomerular inflammation with higher glomerular scores in MRL/lpr mice than in miR-223 knockdown mice, interstitial inflammation was similarly observed between the two groups. IgG deposition in renal had an obvious remission after miR-223 inhibitor treatment (F). The MRL/lpr mice with miR-223 knockdown (20nmol) experienced longer lives (G). The percentage of CD4⁺T cells producing IL-17 A of the spleens in the spleens of BALB/c mice, MRL/lpr and MRL/lpr miR-223 inhibitor group (H). Bars indicate *p < 0.05 analyzed by Student’s unpaired t-test