Baseline levels of IL-6, IL-10, IL-17, IL-23 were increased in patients vs. controls (p < 0.001 for all), as was IFN-γ (p = 0.03). Patients with persisting active nephritis after treatment (WHO III, IV, V) presented higher IL-17 levels at baseline than those who progressed without active nephritis (WHO I-II) (p < 0.03). At follow-up, BILAG-non-responders had higher IL-23 than responders (p < 0.05). This indicates that a subset of LN-patients has a Th17 phenotype that may influence response to treatment. Immunostaining of renal tissue revealed IL-17 expression in inflammatory infiltrates. This evidence concerns the gene IL37 and lobular neoplasia.