Psoriasis, a T-cell mediated chronic dermatosis, has a complex etiopathogenesis. There has been extensive research into the aberrant immune response, which leads to the formation of clinical lesions, and the need for developing better and safer drugs has been unrelenting. The past two decades of research has opened up new areas of the immune pathway that can be targeted in order to control the disease. Therefore, we have seen the emergence of biologics which either target T-cell receptors or inhibit Tumor Necrosis Factor-alpha (TNF-α) or inhibit interleukins (IL) like IL-12, IL-17, IL-17 receptor, and more recently IL-23. Drugs specifically targeting the p19 subunit of IL-23 have shown promising results in the management of chronic plaque psoriasis. This has given way to the development of a new class of biologics, that is, the IL-23p19 inhibitors that have a better safety profile as compared to its predecessors. In this review, we shall scrutinize the role of IL-23 and Th17 cell signaling in the evolution of the psoriatic lesions and summarize the clinical experience with IL-23p19 inhibitors especially mirikizumab in the treatment of chronic plaque psoriasis.
Keywords: IL-23p19 inhibitors; mirikizumab; psoriasis.
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