Second, when using IL-23 as activator, the CD3 and CD28 costimulated PBMC responded with an aberrant ex vivo production of IL-17, which provided robust evidence on the direct involvement of IL-23 in the IL-23/IL-17 inflammatory axis, which acts to induce a distinct T-cell activation state that produces IL-17 as the effector cytokine that promotes the autoinflammatory responses in SLE. The gene discussed is IL17A; the disease is systemic lupus erythematosus.