Fig. 7

Overexpression of Peli1 prevents lupus-like disease. a Immunoblot analysis of p52, p100, NIK, Peli1, Peli1ΔC and HSP60 in Peli1-knockdown M12 cells that reconstituted with empty vector (EV), WT full-length Peli1 or Peli1ΔC that stimulated with anti-CD40 (αCD40) at the indicated time points. b Analysis of Lys48 ubiquitination of NIK in Peli1-knockdown M12 cells reconstituted with EV, WT Peli1, or Peli1ΔC that stimulated with anti-CD40 (αCD40) for 4 h in the presence of MG132. c LISA of NP-specific IgM, IgG2a, IgG2b and IgG3 in the serum of Rag1^−/− mice that transferred with WT T cells plus KO B cells reconstituted with EV, WT Peli1 or Peli1ΔC, and then immunized intraperitoneally with NP-KLH. d–h Peli1-deficient (KO) mice were immunized with 7.5 million of BM12 CD4⁺ T cell to induce lupus-like disease, and then injected with pRV-GFP retrovirus encoding Peli1 or Peli1ΔC 12 h post-immunization. The IgG deposits in kidney were examined by staining with Alexa Fluor 488-labeled anti-mouse IgG (d). Scale bar, 100 μm. The anti-dsDNA, anti-ssDNA, anti-histone IgG in serum were determined by ELISA (e). The percentages of CD19⁻CD138⁺ plasma cells, PD-1⁺CXCR5⁺ Tfh cells (f, g) and infected B220⁺ B cells (h) in spleens were assessed by flow cytometry. 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