In B6.Nba2 congenic lupus mice, Tlr9 deletion led to accelerated lupus with an increased production of anti-nuclear antibodies and augmented lupus nephritis, while disease progression in the Tlr7/9 double-deficient mice was restored to a comparable or even slightly improved level as the parental strain [40]. Here, TLR7 is linked to systemic lupus erythematosus.