International immunopharmacology · 2026
IL-19 promotes psoriasis progression by inhibiting keratinocyte apoptosis via the Bcl-2/Caspase-3 axis.
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Zou Ailing, Pu Qianhan, Chen Yongjun, Zheng Chen, Tong Hui
Аннотация
BACKGROUND: Keratinocyte apoptosis dysregulation is central to psoriasis pathogenesis. Interleukin-19 (IL-19) is upregulated in psoriatic lesions, but its functional role in apoptotic signaling remains unclear. This study investigated the impact of IL-19 on keratinocyte apoptosis and its underlying mechanism via the Bcl-2/Caspase-3 axis.
METHODS: Clinical samples from psoriasis vulgaris patients (n = 34) and healthy controls (n = 32) were analyzed by immunohistochemistry. In vitro experiments employed M5-stimulated HaCaT cells with IL-19 knockdown/overexpression, assessed by CCK-8, flow cytometry, TUNEL, qPCR and Western blot. In vivo, an imiquimod (IMQ)-induced psoriasis-like mouse model was used to evaluate skin inflammation, apoptosis, and pathway modulation.
RESULTS: IL-19 expression was significantly higher in psoriatic epidermis and correlated positively with Psoriasis Area and Severity Index (PASI) scores. In vitro, IL-19 knockdown promoted keratinocyte apoptosis, reduced Bcl-2, and increased cleaved-caspase-3/PARP; these effects were reversed by IL-19 overexpression. In vivo, IL-19 knockdown ameliorated IMQ-induced psoriasiform skin lesions and epidermal hyperplasia while enhancing keratinocyte apoptosis and modulating Bcl-2/cleaved-caspase-3. Conversely, IL-19 overexpression exacerbated the psoriasiform phenotype and suppressed apoptosis.
CONCLUSION: IL-19 promotes epidermal hyperplasia and inhibits keratinocyte apoptosis by regulating the Bcl-2/Caspase-3 signaling axis. These findings not only clarify a key molecular mechanism in psoriasis pathogenesis but also highlight IL-19 and its downstream pathway as promising candidates for targeted therapy.
METHODS: Clinical samples from psoriasis vulgaris patients (n = 34) and healthy controls (n = 32) were analyzed by immunohistochemistry. In vitro experiments employed M5-stimulated HaCaT cells with IL-19 knockdown/overexpression, assessed by CCK-8, flow cytometry, TUNEL, qPCR and Western blot. In vivo, an imiquimod (IMQ)-induced psoriasis-like mouse model was used to evaluate skin inflammation, apoptosis, and pathway modulation.
RESULTS: IL-19 expression was significantly higher in psoriatic epidermis and correlated positively with Psoriasis Area and Severity Index (PASI) scores. In vitro, IL-19 knockdown promoted keratinocyte apoptosis, reduced Bcl-2, and increased cleaved-caspase-3/PARP; these effects were reversed by IL-19 overexpression. In vivo, IL-19 knockdown ameliorated IMQ-induced psoriasiform skin lesions and epidermal hyperplasia while enhancing keratinocyte apoptosis and modulating Bcl-2/cleaved-caspase-3. Conversely, IL-19 overexpression exacerbated the psoriasiform phenotype and suppressed apoptosis.
CONCLUSION: IL-19 promotes epidermal hyperplasia and inhibits keratinocyte apoptosis by regulating the Bcl-2/Caspase-3 signaling axis. These findings not only clarify a key molecular mechanism in psoriasis pathogenesis but also highlight IL-19 and its downstream pathway as promising candidates for targeted therapy.