IL17A and systemic lupus erythematosus: They also contribute to SLE pathogenesis through their direct production of type I IFN [13], or through the highly immunogenic neutrophil extracellular traps (NETs) amplifying the production of either type I IFN [14] or IL-17 [15], although these later findings have been refuted in the MRL/lpr lupus-prone mouse model [16].