STING Signaling Pathway Promotes Autoantibody Production and Glomerulonephritis in the Fcgr2b−/− Lupus Mice
(A)The anti-nuclear antibodies (ANA) were detected in the serum (dilution 1:800) using the immunofluorescence staining on Hep-2 cells (A). Data are representative of eight mice per group (scale bar, 20 μm).
(B) Semi-quantification of ANA was graded by fluorescence intensity (N = 8 mice per group).
(C) Anti-dsDNA from sera (dilution 1:100) of Fcgr2b−/− and Fcgr2b−/−. Stinggt/gt was detected by ELISA (N = 10–11 per group).
(D) Kidney sections of Fcgr2b−/− and Fcgr2b−/−. Stinggt/gt mice (6–8 months old) were stained with H&E. Data are representative of 7–10 mice per group (scale bar, 25 μm).
(E–H) (E and F) Glomerular scores and interstitial scores of kidney sections were blindly graded (N = 7–10 per group). Immunofluorescence staining of the kidneys from Fcgr2b−/− and Fcgr2b−/−. Stinggt/gt mice show in (G) IgG (green), CD45 (red), and DAPI (blue) and (H) C3c (green), CD3 (red), and DAPI (blue). Data are representative of 3–4 mice per group (scale bar, 10 μm).
(I and J) The quantitative immunofluorescence signal (I) CD45, and IgG, (J) CD3 and C3c (N = 3–4 mice per group). Data are shown as mean ± SEM; ∗p < 0.05, ∗∗p < 0.01 and ∗∗∗p < 0.001.
(K) A heatmap of microarray data from the kidneys of Fcgr2b−/− and Fcgr2b−/−. Stinggt/gt mice show that the interferon signature genes significantly changed in the Fcgr2b−/−mice (N = 4 mice per group). Data shown in log2 (sample/wild-type).