IL-36 contributes to enhanced T helper 17 type responses in allergic rhinitis

Background: T helper 17 (Th17) cell subsets, belongs to CD4+ T cell lineage, are proved to be closely related to pathophysiology of AR recently. The interleukin-36 (IL-36) had been reported to promote the up-regulation of Th17 cytokines in psoriasis. We investigated the regulation of Th17 inflammation by IL-36 family cytokines in allergic rhinitis (AR). Methods: Twenty-one patients with AR and 20 healthy controls were enrolled. The expression of serum protein and mRNA of IL-36 family cytokines between AR and control group were detected and compared. Human peripheral blood mononuclear cells were purified and stimulated by IL-36 cytokines. The transcription factor and production of Th17 cytokines by Th17 cells were evaluated. Mouse model with AR was established to confirm the in vitro results. Results: The serum expression of IL-36 cytokines and Th17 cytokines (IL-17 and IL-23) of AR patients were upregulated significantly compared with controls. The IL-36 alpha promoted the differentiation and function of Th17 cells. The anti-IL-36 alpha treatment could alleviate the Th17 response in AR mice, presented with alleviated symptoms, decreased infiltration of Th17 cells and down-regulated Th17 cytokines expression. Conclusions: IL-36 alpha was involved in the regulation of Th17 responses in allergic rhinitis.