IL-35 Inhibited Th17 Response in Children with Allergic Rhinitis.

OBJECTIVE:Previous studies have proved that Th17 (T helper 17) cell subsets, a unique proinflammatory CD4+ T cell lineage, are deeply involved in the pathophysiology of allergic rhinitis (AR). IL-35, secreted mainly by natural Treg (nTreg) and depending on the expression of Foxp3, can effectively alleviate allergen-induced specific airway inflammation. However, the regulation of IL-35 in AR is not clear. METHODS:Twenty AR children and 20 healthy controls were enrolled. The expression of serum IL-35 protein was detected and the correlation with Th17 cytokines (IL-17, IL-23, IL-27) expression was analyzed by enzyme-linked immunosorbent assay (ELISA). Peripheral blood mononuclear cells were prepared and stimulated by IL-35 to explore its effect on Th17 inflammation. RESULTS:Serum IL-35 levels in AR were negatively correlated with serum IL-17 and IL-23 levels in AR. Recombinant IL-35 inhibits the Th17 response of PBMCs, which were mediated by the mitogen-activated protein kinase (MEK) and c-Jun N-terminal kinase (JNK) pathways. CONCLUSIONS:Our data demonstrate that IL-35 can inhibit Th17 response in AR through MEK and JNK pathways.

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