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Kahlenberg and coworkers have reported in ARD that interferon kappa (IFN-κ) is a key regulator of type I interferon (IFN) photosensitive responses in patients with cutaneous lupus erythematosus (CLE).
They analyzed mRNA expression of type I IFN gene expression by microarrays of biopsied CLE lesions and healthy control skin. They also examined gene expression in cultured keratinocytes, fibroblasts and endothelial cells IFNK knock-out keratinocytes generated using CRISPR/Cas9.
They discovered that IFNK is one of two type I IFNs significantly increased (1.5-fold change) in lesional CLE skin.
Type I IFN responses were enriched in keratinocytes, but not in fibroblast or endothelial cells, and that epithelial-derived IFN-κ is responsible for maintaining baseline type I IFN responses in healthy skin.
Increased levels of IFN-κ seen in SLE can amplify and accelerate responsiveness of epithelia to IFN-α and increase keratinocyte sensitivity to UV irradiation.
IFN-κ is a critical IFN in CLE pathology via promotion of enhanced IFN responses and photosensitivity and could therefore be a potential novel treatment target.