Different expression patterns of plasma Th1‐, Th2‐, Th17‐ and Th22‐related cytokines correlate with serum autoreactivity and allergen sensitivity in chronic spontaneous urticaria

Background Clinical features and basophil activation levels correlate with serum autoreactivity and allergen sensitivity in patients with chronic spontaneous urticaria (CSU). Objectives To explore the relationship of the expression patterns of plasma T-helper cell (Th) 1-, Th2-, Th17- and Th22-related cytokines with the serum autoreactivity and the allergen sensitivity in CSU. Method Twenty related cytokines were measured and analysed in 60 patients with CSU, 15 patients with acute urticaria, 10 patients with atopic dermatitis (AD) and 15 healthy persons, respectively. Autologous serum skin testing (ASST) and skin prick testing (SPT) were performed to detect autoreactivity and allergy sensitivity, respectively. The protein–protein interaction of cytokines and the molecular pathways were analysed by Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and KyotoEncyclopedia of Genes and Genomes (KEGG database), respectively. Results Th1-/Th2- and Th17-related cytokines were significantly elevated and correlated with disease activity in CSU than in healthy controls. Interleukin (IL)-6, IL-10 and IL-13 were significantly higher in acute urticaria than in patients with CSU. Granulocyte/macrophage colony-stimulating factor (GM-CSF), IL-10 and IL-17 were significantly higher in ASST+ than in ASST- CSU patients. IFN-γ, IL-2, IL-12p70 and IL-21 were significantly higher in SPT+ than in SPT− CSU patients. The plasma levels of interferon-γ, IL-2 and IL-21 varied among ASST+/SPT+, ASST+/SPT−, ASST−/SPT+ and ASST−/SPT− CSU subgroups, which appeared to involve the positive regulation of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. Conclusion This study indicates acute urticaria elicits a more prominent Th2 immune response than CSU. There was association between different expression patterns of plasma Th1-, Th2-, Th17- and Th22-related cytokines and serum autoreactivity or allergen sensitivity in CSU. Further studies on the JAK-STAT pathway in the pathogenesis of CSU are warranted.