Abstract
Abstract Systemic lupus erythematosus (SLE) often involves kidney damage, and the inflammasome-caspase-1 cascade had been demonstrated promoting renal pathogenesis. However, our present work found that deficiency of Aim2 led to enhanced nephritis in pristane-induced experimental lupus model. We further found that increased type I interferon (IFN-I) signal in the Aim2−/− mice was in tandem with exaggerated SLE. Moreover, adaptive immune cells were also involved in the interstitial nephritis in the glomeruli of Aim2−/− mice. Of note, even without pristine challenge, Plasmacytoid dendritic cells in the kidney of Aim2−/− mice were significantly more abundant compared with control animals. A transcriptome analysis revealed that Aim2 deficiency led to enhanced expression of IFN-I-induced genes in the kidney at different developmental stages. Taken together, our study demonstrates a critical role for AIM2 in suppressing IFN-I production and development of SLE.
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