Abstract
The development of psoriasis, a common, chronic inflammatory skin disease, significantly depends on interleukin (IL)-17 (1). Anti-IL-17 inhibitors, such as ixekinumab (anti-IL-17A antibody), secukinumab (anti-IL-17A antibody) and brodalumab (anti-IL-17 receptor A (IL-17RA) antibody) exert excellent therapeutic effects on psoriasis (2). On the other hand, since IL-17 is an important cytokine for preventing fungal infections, skin side effects such as cutaneous candidiasis are occasionally seen during the administration of IL-17 inhibitors (3).
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