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. 2022 Jan 24;13(1):81. doi: 10.1038/s41419-022-04523-3

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Cytokines are essential in the pathogenesis of psoriasis. Recently, cytokines derived from or receptors expressed on keratinocytes have shown great importance in psoriasis. Keratinocytes are critical cytokine responders in psoriasis, as keratinocyte-specific deletion of their receptors (such as IL-17RA and IL-36R) alleviated psoriasiform lesion in psoriatic mouse model. Keratinocyte-derived IL-17C, IL-17E, IL-36, and IL-23 could induce expression of proliferative and proinflammatory genes by multiple signaling pathways, leading to epidermal hyperplasia and amplification of inflammation and leukocyte infiltration. IL-17RA IL-17 receptor A, TRAF6 TNF receptor-associated factor 6, IL-36R IL-36 receptor, IL-1RAcp IL-1 receptor accessory protein, TWEAK tumor necrosis factor (TNF)-like weak inducer of apoptosis, Fn14 factor-inducible 14, IL-22BP IL-22 binding protein.