Pristane, a mineral oil component, induces SLE models primarily by activating B cells in the immune system. The disease progression in this model more closely resembles the chronic onset of human SLE, but the modeling period is relatively long.
Imiquimod (IMQ) acts mainly by activating TLR7, rapidly initiating an immune response. The disease onset is relatively fast with a short modeling time, although its systemic manifestations may not be as comprehensive or severe as those in the pristane‑induced model.
Based on the above principles, The SMOC has established an SLE model by combining nephrectomy with pristane and IMQ induction, and has validated the phenotypes in different strains (hCD3EDG/hCD19, BALB/c, etc.). This model exhibits rapid onset, significantly shortening the modeling time, with prominent phenotypes, and can be used for efficacy evaluation of antibody‑based drugs for SLE.
Fig.1 IMQ and Pristane induce nephrectomy Balb/c mice SLE model. (A) Body weight. (B) Body weight change.
Fig.2 Serum anti-dsDNA IgG Ab of IMQ and Pristane induce nephrectomy Balb/c mice SLE model.
Fig.3 IMQ and Pristane induce nephrectomy Balb/c mice SLE model. (A) mCD45+ cells in live cells proportion. (B) mCD20+ cells in live cells proportion. (C) mCD20+ cells in mCD45+ cells proportion.
Fig.4 IMQ and Pristane induce nephrectomy Balb/c mice SLE model. (A) Urine Albumin. (B) Urine Creatinine. (C) Albumin to creatinine ratio.
Fig.5 IMQ and Pristane induce nephrectomy Balb/c mice SLE model. (A) Spleen index. (B) Kidney index.
Fig.6 IMQ and Pristane induce nephrectomy Balb/c mice SLE model. (A) Representative H&E staining. (B) Histopathology score.
Fig.7 IMQ and Pristane induce nephrectomy Balb/c mice SLE model. (A) mIgG IHC staining. (B) % mIgG positive cells.
Pristane, a mineral oil component, induces SLE models primarily by activating B cells in the immune system. The disease progression in this model more closely resembles the chronic onset of human SLE, but the modeling period is relatively long.
Imiquimod (IMQ) acts mainly by activating TLR7, rapidly initiating an immune response. The disease onset is relatively fast with a short modeling time, although its systemic manifestations may not be as comprehensive or severe as those in the pristane‑induced model.
Based on the above principles, The SMOC has established an SLE model by combining nephrectomy with pristane and IMQ induction, and has validated the phenotypes in different strains (hCD3EDG/hCD19, BALB/c, etc.). This model exhibits rapid onset, significantly shortening the modeling time, with prominent phenotypes, and can be used for efficacy evaluation of antibody‑based drugs for SLE.
Fig.1 IMQ and Pristane induce nephrectomy hCD3EDG/hCD19 mice SLE model. (A) Body weight. (B) Body weight change.
Fig.2 IMQ and Pristane induce nephrectomy hCD3EDG/hCD19 mice SLE model. (A) Serum BUN. (B) Serum CRE. (*P<0.05, **P<0.01 Vs Group2)
Fig.3 IMQ and Pristane induce nephrectomy hCD3EDG/hCD19 mice SLE model. (A) Serum anti-dsDNA IgG Ab on Day 28. (B) Serum anti-dsDNA IgG Ab on Day 68.
Fig.4 IMQ and Pristane induce nephrectomy hCD3EDG/hCD19 mice SLE model. (A) mCD45 cells in live cells proportion. (B) mCD20 cells in live cells proportion. (C) mCD20 cells in mCD45 cells proportion.
Fig.5 IMQ and Pristane induce nephrectomy hCD3EDG/hCD19 mice SLE model. (A) Urine Albumin. (B) Urine Creatinine. (C) Albumin to creatinine ratio. (*P<0.05,**P<0.01 Vs Group2)
Fig.6 IMQ and Pristane induce nephrectomy hCD3EDG/hCD19 mice SLE model. (A) Spleen photo and Kidney photo. (B) Spleen index and Kidney index. (**P<0.01 Vs Group2)
Fig.7 IMQ and Pristane induce nephrectomy hCD3EDG/hCD19 mice SLE model. (A) Representative H&E images in SLE model. (B)Histopathology score. (*P<0.05 Vs Group2)
Fig.9 IMQ and Pristane induce nephrectomy hCD3EDG/hCD19 mice SLE model. (A) Representative IHC images in SLE model. (B) % mIgG positive cells.
The humanized SLE model is established by transferring peripheral blood mononuclear cells (PBMCs) from SLE patients into immunodeficient mice. This model helps to better understand the characteristics of human SLE and can be used for preclinical testing of antibodies, small molecules, and other drugs, thereby accelerating translational research.
Fig1. The model of systemic lupus erythematosus induced by SLE-PBMCs in M-NSG mice. (A) Body weight curve. (B) Anti-dsDNA IgG curve. (C) Renal index. (D) Proportion of human CD45+ cells among all CD45+ cells 14 days after immune reconstitution.
Fig2. The efficacy of Blinatumomab on SLE-PBMC induced SLE model in M-NSG mice. (A–H) Changes in the numbers of various immune cells in peripheral blood 7–28 days after immune reconstitution. (I) Time course of anti-dsDNA IgG. (J) Renal index. The results indicate that the monoclonal antibody blinatumomab significantly reduced the number of immune cells, anti-dsDNA IgG levels and the renal index in the SLE-PBMC-induced systemic lupus erythematosus model.
Fig.1 Body weight of SLE model in BALB/c and C57BL/6 mice.
Fig.2 SLE model in BALB/c and C57BL/6 mice. (A) Serum anti-dsDNA IgG Ab at 6 weeks post administration, (B) Serum anti-dsDNA IgG Ab at 12 weeks post administration.
Fig.3 HE staining results and analysis of the SLE model. (*P<0.05,***P<0.001)
