MRL/lpr is another widely used spontaneous animal model for systemic lupus erythematosus (SLE), and its clinical manifestations are highly similar to those of human lupus erythematosus. The MRL/lpr mouse strain was developed by Murphy and Roths at the Jackson Laboratory in the United States in 1978. It was generated through a series of complex intercrosses among multiple mouse strains including LG/J, AKR/J, C3H/D and C57BL/6, and stabilized at the 12th generation. Its alloantigen and phenotypic characteristics are H-2ᵏ, Lyt-1.2⁺, Lyt-3.1⁺ and TLT positivity. Genetically, MRL/lpr mice inherit 75% genetic background from LG/J, 12.6% from AKR/J, 12.1% from C3H/D, and 0.3% from C57BL/6. This strain carries a recessive mutation in the Fas gene, which is critical for spontaneous cellular apoptosis. The mutation triggers lymphoproliferation, excessive T cell expansion and generalized lymphadenopathy, thereby exacerbating autoimmune responses. Pathological and serological features include erosive arthritis, elevated autoantibodies such as anti-DNA, anti-Sm, anti-Su and anti-nucleoside P antibodies, high-titer antinuclear antibody (ANA), hypergammaglobulinemia, and rheumatoid factor (RF) detected in half of the individuals. Renal lesions manifest as subacute proliferative glomerulonephritis with mild to moderate proteinuria. The disease incidence shows no gender preference, with a 50% mortality rate occurring at the fifth month of age.

Male C57BL/6 mice and male MRL/lpr mice
Modeling method: Pathological examinations were performed after feeding up to 22 weeks of age, with obvious disease onset observed at 15 weeks.
Evaluation indexes: urine protein detection, HE staining, PAS staining

Urine protein detection

Renal tissue HE staining

Renal tissue PAS staining