Supplemental Fig 1 for "Persistent expression of IL-17 and downstream cytokines after ustekinumab treatment in patients with psoriasis"

Published: 16 April 2020| Version 2 | DOI: 10.17632/h2pjwzbk8j.2
Contributor:
Sang Woong Youn

Description

Background : The interleukin (IL)-23/T helper (Th)17 axis is considered central to the pathogenesis of psoriasis. However, expression data regarding key cytokines in the pathogenesis of psoriasis, as well as data on the effects of IL-23 inhibition on downstream cytokines in human psoriatic skin, are limited. Object : The purpose of this study was to evaluate the effect of ustekinumab on cytokine expression in a human psoriasis tissue. Methods : We investigated the expression profile of key cytokines and the effect of ustekinumab on cytokine expression in human psoriatic tissue. Results : Tumor necrosis factor (TNF)-α, IL-23, IL-17A, and IL-22 were highly expressed in the epidermis and upper dermis in patients with psoriasis; IL-36γ was strongly expressed in the upper epidermis. Expression intensity and area of IL-23 were significantly decreased in the ustekinumab treated group; expression areas of TNF-α, IL-17A, IL-22, and IL-36γ did not differ. Limitation : Conclusion : This study identified that ustekinumab improves psoriasis by downregulating IL-23 without blocking downstream cytokines. Our results suggest that, although IL-23 is inhibited, the persistent expression of IL-17 through an alternative pathway maintains the vicious cycle of TNF-α/IL-23/IL-17 axis with IL-36γ, inducing refractory psoriatic lesions in patients with well-controlled psoriasis.

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