Abstract
Psoriasis is a common skin disease accompanied by chronic inflammation. In previous studies, erythroid differentiation regulator 1 (ERDR1) was shown to have a negative correlation with proinflammatory cytokine IL-18. However, the role of ERDR1 in the inflammatory skin disease psoriasis has not been evaluated. In this study, to investigate the role of ERDR1 in psoriasis, recombinant ERDR1 was injected intraperitoneally into a psoriasis mouse model. Recombinant ERDR1 (rERDR1) significantly alleviated the symptoms of psoriasis-like skin inflammation and reduced the mRNA of various psoriasis-related markers, including keratin 14, S100A8, and Th17-related cytokines IL-17 and IL-22, suggesting that rERDR1 exerts therapeutic effects on psoriasis via the regulation of Th17 functions. Additionally, the expression of CCL20, a well-known Th17 attracting chemokine, was determined. CCL20 expression significantly decreased in the rERDR1-injected group compared with the vehicle (PBS)-injected group. CCR6 expression in the psoriatic lesional skin was also decreased by rERDR1 administration, implying the inhibition of CCR6-expressing Th17 cell chemotaxis via the downregulation of CCL20. Taken together, this study provides the first evidence that ERDR1 may be a potential therapeutic target for psoriasis.
Highlights
Psoriasis is a common chronic skin disease that affects 2%–3% of the world’s population and manifests as red and white scaly plaques on the top layer of the skin
To investigate the therapeutic effect of erythroid differentiation regulator 1 (ERDR1) on psoriasis, Aldara cream containing 5% imiquimod was topically applied to the shaved back skin of C57BL/6J mice to induce a psoriasis-like skin inflammation, and 10 or 100 μg/kg of recombinant ERDR1 was administered by intraperitoneal (i.p.) injection
Based on increasing evidence for the importance of the CCR6+ Th17 cell population in psoriasis, we suggest that a decreased distribution of CCR6+ Th17 cells in psoriatic lesional skin via the regulation of CCL20 may be a critical mechanism for ERDR1-regulated psoriasis
Summary
Psoriasis is a common chronic skin disease that affects 2%–3% of the world’s population and manifests as red and white scaly plaques on the top layer of the skin. The pathogenesis of psoriasis is not fully understood, studies have demonstrated the involvement of immune-mediated cutaneous inflammation. Various stimuli such as stress, infection, and allergens stimulate keratinocytes to produce cytokines and chemokines in the dermal region, which trigger the extravasation of immune cells from blood vessels to lesional sites [1]. Because the onset and maintenance of psoriasis is mediated by various inflammatory cytokines, therapeutic approaches focus on inhibition of certain inflammatory responses to improve disease symptoms [3,4]
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