Therapeutic JAK1 inhibition reverses lupus nephritis in a mouse model and demonstrates transcriptional changes consistent with human disease

Janus kinase family members are essential for signaling by multiple cytokines, including many implicated in SLE pathogenesis. To test whether inhibition of JAK1 signaling can be efficacious in SLE, we used a JAK1-selective inhibitor (ABT-317) and evaluated its ability to ameliorate disease in murine SLE. 48 NZB/W-F1 mice were treated with anti-CD40 or anti-JAK1 and kidney and salivary gland tissue were used for NA extraction. Young mice and baseline (disease onset) mice were used as controls.