Fig. 5
From: Peli1 negatively regulates noncanonical NF-κB signaling to restrain systemic lupus erythematosus
The noncanonical NF-κB pathway is required for lupus pathology in Peli1-deficient mice. a–c Rag1-dificient mice (recipient, R) were adoptively transferred with WT or KO B cells (donor, D), and then immunized with BM12 CD4+ T cell. The IgG deposits in kidney were determined by staining with Alexa Fluor 488-labeled anti-mouse IgG (a, Scale bar, 100 μm), the serum ANA were analyzed by using the Hep-2 cell line (b), and the anti-dsDNA, anti-ssDNA, anti-histone IgG in serum were examined by ELISA (c). d Proliferation of WT and KO splenic B cells that infected with control or NIK shRNA, incubated in vitro for 72 h in the absence (NT) or presence of anti-CD40 or BAFF, then assessed by [3H]thymidine incorporation. e–g Rag1-dificient mice were adoptively transferred with WT or KO B cells that infected with control or NIK shRNA, and then immunized with BM12 CD4+ T cell. The kidney IgG deposition were visualized with Alexa Fluor 488-labeled anti-mouse IgG (e, Scale bar, 100 μm), the serum ANA were analyzed by using the Hep-2 cell line (f, Scale bar, 50 μm.), and the anti-dsDNA, anti-ssDNA, anti-histone IgG in serum were examined by ELISA (g). Ctrl, control. Data are shown as the mean ± SEM based on three independent experiments. Two-tailed Student’s t-tests were performed. *P < 0.05 and **P < 0.01
