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The following is a summary of “Solar urticaria involves rapid mast cell STAT3 activation and neutrophil recruitment, with FcεRI as an upstream regulator,” published in the May 2024 issue of Allergy & Immunology by Rutter, et al.
Solar urticaria, characterized by sunlight-induced urticaria, remains poorly understood in terms of its pathophysiology. For a study, researchers sought to delineate the cellular and molecular events in developing solar urticaria following solar-simulated UV radiation (SSR) exposure and compare them with healthy controls (HC).
Skin biopsy specimens were obtained from unexposed skin and skin exposed to a single low dose of SSR at 30 minutes, 3 hours, and 24 hours post-exposure in 6 patients with solar urticaria and 6 HC. Immunohistochemistry and bulk RNA-sequencing analysis were performed on the biopsy specimens.
Several innate immune pathways were enriched in solar urticaria specimens, with early involvement of neutrophils not observed in HC. Upregulation of multiple proinflammatory cytokine and chemokine genes (e.g., IL20, IL6, CXCL8) and identification of upstream regulators (e.g., TNF, IL-1β, IFN-γ) were noted. IgE and FcεRI were identified as early regulators, with increased expression of phosphorylated signal transducer and activator of transcription 3 in mast cells at 30 minutes and 3 hours post-SSR exposure, suggesting mast cell activation. Clinical resolution of solar urticaria by 24 hours paralleled resolution of inflammatory gene signature profiles. Comparison with chronic spontaneous urticaria datasets revealed transcriptomic similarities in immune activation, with unique transcripts identified solely in solar urticaria.
Solar urticaria is characterized by rapid mast cell activation involving signal transducer and activator of transcription 3, along with multiple chemotactic and innate inflammatory pathways. FcεRI engagement appeared to be an early event in the pathogenesis of solar urticaria.
Reference: jacionline.org/article/S0091-6749(24)00006-X/fulltext
