Clinical immunology (Orlando, Fla.) · 2026
CLIC1 acts as a compensatory protective molecule to regulate the vascular endothelial barrier integrity in cutaneous inflammation.
СтатьяНазвание и аннотация: Перевод в очереди
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Zheng Xinlin, Liu Yucong, Luo Qi, Shen Zhu
Аннотация
BACKGROUND: Vascular dysfunction is common in inflammatory skin disorders, but its regulation remains unclear.
METHODS: Through bioinformatics, we identified CLIC1 upregulation in psoriasis and atopic dermatitis endothelial cells. Using gain- and loss-of-function assays in endothelial cells, alongside transcriptomics, human skin biopsies, and an imiquimod-induced psoriasis mouse model, we investigated CLIC1's functional role.
RESULTS: CLIC1 overexpression enhanced endothelial barrier integrity and reduced neutrophil transmigration, whereas CLIC1 knockdown had opposite effects. Mechanistically, CLIC1 regulated tight junction protein 2 (TJP2), which was required for its protective effect. Human lesions showed CLIC1 and TJP2 co-upregulation with TJP2 redistributing to reinforce the barrier. In vivo, CLIC1 overexpression ameliorated psoriasiform dermatitis.
CONCLUSION: CLIC1 acts as a compensatory barrier-protective molecule in inflamed endothelium and represents a potential therapeutic target for inflammatory skin disorders.
METHODS: Through bioinformatics, we identified CLIC1 upregulation in psoriasis and atopic dermatitis endothelial cells. Using gain- and loss-of-function assays in endothelial cells, alongside transcriptomics, human skin biopsies, and an imiquimod-induced psoriasis mouse model, we investigated CLIC1's functional role.
RESULTS: CLIC1 overexpression enhanced endothelial barrier integrity and reduced neutrophil transmigration, whereas CLIC1 knockdown had opposite effects. Mechanistically, CLIC1 regulated tight junction protein 2 (TJP2), which was required for its protective effect. Human lesions showed CLIC1 and TJP2 co-upregulation with TJP2 redistributing to reinforce the barrier. In vivo, CLIC1 overexpression ameliorated psoriasiform dermatitis.
CONCLUSION: CLIC1 acts as a compensatory barrier-protective molecule in inflamed endothelium and represents a potential therapeutic target for inflammatory skin disorders.