JOURNAL ARTICLE

P27 Chloride intracellular channel 4 is a global regulator of type 1 interferon signalling in systemic sclerosis skin.

  • Published In: British Journal of Dermatology, 2024, v. 190, n. 6. P. e91 1 of 3

  • Database: Academic Search Ultimate 2 of 3

  • Authored By: Wasson, Christopher; Dibb, Sophie; Bryon, Jessica; Caballero-Ruiz, Begoña; Clavane, Eva; Wells, Rebecca; Kakkar, Vishal; Lorenzis, Enrico De; Ross, Rebecca; Meakin, Paul; Galdo, Francesco Del 3 of 3

Abstract

This article focuses on the role of chloride intracellular channel 4 (CLIC4) in systemic sclerosis (SSc), an autoimmune disease characterized by skin fibrosis and potential internal organ involvement. The study found that CLIC4 expression is elevated in skin fibroblasts, keratinocytes, and endothelial cells of SSc patients compared to healthy controls, and that CLIC4 regulates type 1 interferon (IFN) signaling in keratinocytes. Inhibition of CLIC4 blocked activation of the IFN signaling pathway transcription factor STAT1 mediated by Toll-like receptors and cGAS, and prevented SSc fibroblast-induced IFN responses in keratinocytes. These findings suggest that CLIC4 acts as a global regulator of type 1 IFN signaling in epithelial cells affected by SSc.

Additional Information

  • Source:British Journal of Dermatology. 2024/06, Vol. 190, Issue 6, pe91
  • Document Type:Article
  • Subject Area:History
  • Publication Date:2024
  • ISSN:0007-0963
  • DOI:10.1093/bjd/ljae105.049
  • Accession Number:177358796
  • Copyright Statement:Copyright of British Journal of Dermatology is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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