IL17A and systemic lupus erythematosus: Studies in interleukin-23 (IL-23)–deficient mice suggest that the IL-23/IL-17 axis promotes such kidney inflammation 4, and, perhaps reflecting this, expanded populations of Th17- and IL-17–producing CD3+CD4−CD8− T cells are observed in the kidneys of both lupus-prone mice and patients with SLE 5.