Tlr5 deficiency exacerbates lupus-like disease in the MRL/lpr mouse model

We hypothesized that bacterial flagellin-mediated activation of TLR5 would trigger SLE-like autoimmunity in lupus-prone MRL/lpr mice. To provide a comprehensive exploration of the intricate relationship between a leaky gut, flagellin-TLR5 signaling, and their potential impact on the development and progression of disease in SLE, we have assessed the development of autoimmune disease in our newly generated Tlr5-deficient lupus-prone MRL/lpr mice.