Toll-like receptor (TLR) 7 signaling pathway plays an important role in the pathogenesis of Systemic Lupus Erythematosus (SLE). In a recent study, a TLR7 gain-of-function variant (Y264H) was identified in SLE patients. TLR7Y264H led to aberrant activation of TLR7, which in turn over-activated B-cells, leading to the development of SLE[1].
GemPharmatech has independently developed a BALB/c-Tlr7Y264H mouse model, in which mouse Tlr7Y264H mutation was introduced. BALB/c-Tlr7Y264H mice at 12-16 weeks of age developed a spontaneous SLE phenotype, including increased level of serum anti-dsDNA and nephritis. This is an ideal mouse model to study the pathogenesis of SLE and test potential therapeutics that suppress overactivation of TLR7 signaling.
Phenotype data of BALB/c-Tlr7Y264H mouse
a
Serum anti-dsDNA antibody ELISA test of 12 to 16 weeks old BALB/c-Tlr7Y264H mice.
b 
Analysis of kidney H&E staining in 12 to 16 weeks old BALB/c-Tlr7Y264H mice.
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[1] Brown GJ.et al. TLR7 gain-of-function genetic variation causes human lupus. Nature.
2022 May;605(7909):349-356.