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Article Abstract
Psoriasis, a common inflammatory skin disease, is critically dependent on the IL-23/IL-17 cytokine axis. Although immune cell-derived IL-23 is generally associated with the disease pathogenesis, there have been reports of IL-23 production in keratinocytes. To determine the presence and potential role of keratinocyte-derived IL-23 in psoriasis, we investigated its expression levels using publicly available single-cell RNA sequencing data from human samples. We discovered that the expression of IL23A was detectable in keratinocytes as well as dendritic cells. Furthermore, we examined the IL-23p19 expression in an imiquimod-induced mouse model of psoriasis and found a close relationship between keratinocyte-produced IL-23 and IL-36, another key cytokine in psoriasis pathogenesis. The blockade of IL-23 signaling resulted in the reduced expression of IL-36 in the keratinocytes. Our findings reveal the novel association between keratinocyte-derived IL-23 and IL-36 in psoriasis progression.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9174585 | PMC |
| http://dx.doi.org/10.3389/fimmu.2022.905239 | DOI Listing |
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Article Synopsis
- Psoriasis is heavily influenced by the IL-23/IL-17 cytokine axis, with IL-23 typically produced by immune cells, but this study also focused on its production by keratinocytes (skin cells).
- Using single-cell RNA sequencing data, researchers found that keratinocytes and dendritic cells both express IL23A, indicating that keratinocytes may play a role in psoriasis.
- In a mouse model of psoriasis, they discovered that keratinocyte-derived IL-23 is linked to IL-36 levels, and blocking IL-23 signaling decreased IL-36 expression, highlighting a potential new pathway in psoriasis progression.
Multifaceted Analysis of IL-23A- and/or EBI3-Including Cytokines Produced by Psoriatic Keratinocytes.
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