Systemic Lupus Erythematosus (SLE)

Panel A Transgenic high expression of human BAFF in mice improved the level of IgA, IgM, IgG  and anti-dsDNA IgG in the serum continuously , which were significantly higher than those of the control group mice.

Panel B Increased lupus nephritis activity and chronicity index were observed in B6-hBAFF mice.

Statistical analysis was performed using one‑way ANOVA, and all data are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001

Panel A Rituximab treatment significantly reduced serum levels of anti-dsDNA IgG, total IgG, and IgM.

Panel B Urinary albumin-to-creatinine ratio (UACR) and urinary protein-to-creatinine ratio (UPCR) were decreased following rituximab treatment.

Panel C Rituximab treatment reduced both the lupus nephritis activity index and the proportion of PAS-positive staining.

Statistical analysis was performed using one‑way ANOVA, and all data are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001，****p<0.0001

Panel A In both female and male mice aged 7 to 21 weeks, serum anti-dsDNA levels were significantly higher in B6-Trex1-KO mice compared to control B6 mice. This result aligns with the previously described autoimmune phenotype of TREX1-deficient mice, where genomic DNA accumulation triggers autoimmune responses characteristic of SLE pathogenesis.

Panel B An increased interferon-stimulatory DNA (ISD) response was observed in heart tissue of TREX-1 KO mice at 32 weeks of age.

Statistical analysis was performed using one‑way ANOVA, and all data presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001，****p<0.0001

Panel A Study design for the efficacy study of upadacitinib in TREX-1 KO mice.

Panel B Upadacitinib treatment improved the survival rate of TREX-1 KO mice.

Panel C Anti-dsDNA IgG levels were significantly reduced following upadacitinib administration.

Panel D Upadacitinib alleviated elevated LDH levels in TREX-1 KO mice.

Panel E Heart tissues harvested at study endpoint for pathological analysis. Upadacitinib treatment markedly lowered histological HE scoring.

Statistical analysis was performed using one‑way ANOVA, and all data presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001，****p<0.0001

Panel A Study design of TLR7 agonist-induced SLE mouse model establishment

Panel B Serum anti-dsDNA antibody levels were elevated in the TLR7 agonist treatment group in both B6 and BALB/c mice.

Panel C  Multiple immune cell populations were expanded in TLR7 agonist-induced SLE model mice of BALB/c background.

Panel D  Renal pathological scores and inflammatory infiltration scores were significantly higher in the model group.

Statistical analysis was performed using one‑way ANOVA, and all data presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001，****p<0.0001

Panel A Study design: Efficacy study in TLR7 agonist-induced SLE mouse model

Panel B Enpatoran reduced urinary protein levels at Day 47 post-dose

Panel C Anti-dsDNA IgG levels were decreased following 47 days of prednisolone treatment

Panel D Renal pathological scores were reduced at Day 49 post Enpatoran administration

Panel E Splenic B cells and DCs were decreased after 49 days of treatment with prednisolone and Enpatoran

Statistical analysis was performed using one‑way ANOVA, and all data presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001，****p<0.0001

Panel A Study design: Efficacy evaluation in human SLE patient PBMC-engrafted NCG mice

Panel B Anti-dsDNA IgG levels were reduced following 7-day and 21-day treatment with anti-CD20 antibody and CD3×CD19 TCE.

Panel C  Splenic B cells and plasma cells were markedly decreased after 21 days of anti-CD20 antibody and CD3×CD19 TCE treatment.

Panel D  Renal IgG deposition was attenuated following 21-day administration of anti-CD20 antibody and CD3×CD19 TCE.

Statistical analysis was performed using one‑way ANOVA, and all data are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001，****p<0.0001