Psoriasis is a common, chronic inflammatory skin disease and cannot be cured. The treatment of moderate-to-severe plaque psoriasis has been revolutionized with the development of biologic agents for nearly 20 years. Current studies show that interleukin-23 and interleukin-17 play remarkable roles in the pathogenesis of psoriasis. Interleukin-23 can sustain the differentiation and maintenance of T helper-17 lineage. Interleukin-17 can recruit and stimulate many cells, which play important parts in psoriasis through interacting with the interleukin-17 receptor. Several biologic agents targeting interleukin-23, interleukin-17, or their receptors are now in different stages: some are approved or clinical trials are in progress. Ustekinumab targets interleukin-23/interleukin-12p40; risankizumab, guselkumab, and tildrakizumab target interleukin-23p19; secukinumab and ixekizumab target interleukin-17A; and brodalumab targets the interleukin-17 receptors. All of these agents have good efficacy in treating moderate-to-severe psoriasis.