Clinical efficacy of selective JAK1 inhibition and transcriptome analysis of chronic discoid lupus erythematosus.
Andreea CalugareanuC GrolleauH Le BuanecF ChassetM JachietM BattistellaMartine BagotD JullienS PoutrelJean-David BouazizB Ben SaidPublished in: Journal of the European Academy of Dermatology and Venereology : JEADV (2021)
Chronic discoid lupus erythematosus (CDLE) is the most common subtype of chronic cutaneous lupus erythematosus (CCLE), and may be associated with systemic lupus manifestations1 . Type I interferons (IFNs) have been identified to play a key role in its pathogenesis2,3 . Following exposure to nuclear components (such as endogenous nucleic acid) released by cellular damage, plasmacytoid dendritic cells (pDC) and keratinocytes inadequately produce type I IFN. In an autocrine loop manner IFNs will bind to IFN-α/β receptors and will activate Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway, thus enhancing expression of proinflammatory mediators (e.g., CXCL10)2,4 .