Abstract
Objectives Interleukin-27 (IL-27) has been reported to inhibit type 2 T helper cell (Th2) response in allergic rhinitis (AR). However, its effects on group II innate lymphoid cells (ILC2) in AR are not fully understood. Methods Nineteen patients with AR and nineteen controls were enrolled in this study. The effects of IL-27 on ILC2 differentiation and function as well as the regulation of the IL-27 receptor (IL-27R) were analyzed by tritiated thymidine incorporation, enzyme-linked immunosorbent assay (ELISA), and real-time polymerase chain reaction (PCR), respectively. AR mice were used to confirm the role of IL-27 in vivo. Results The serum IL-27 protein expression in AR patients was significantly lower compared with controls. IL-27 decreased the ILC2 proliferation and type II cytokine secretion through the interaction with IL-27R. IL-27 also inhibited systemic and nasal ILC2 response of AR mice. Conclusion IL-27 inhibited the proliferation and function of ILC2 in AR, implying that IL-27 may be used as new treatment target in AR.
Highlights
Allergic rhinitis (AR), one of the most common diseases in otorhinolaryngology, affects 10%-20% of the whole population [1]
Enhanced allergic inflammation is found in mice deficient in IL-27 receptor α (IL-27Rα) [11]
We aimed to explore the role of IL-27 on ILC2 differentiation and type II cytokine production using cell and animal models
Summary
Allergic rhinitis (AR), one of the most common diseases in otorhinolaryngology, affects 10%-20% of the whole population [1]. The IL-27 receptor consists of glycoprotein 130 (gp130) and WSX-1 [4]. Previous studies showed that IL-27 can induce type 1 T helper cell (Th1) inflammation, inhibit Th17 response, and induce IL-10producing Foxp3−CD4 T cells [5,6,7]. In Th2-related allergic diseases, IL-27 was reported to inhibit Th2 cell differentiation both in vitro and in vivo and type II cytokine production from Th2 effector cells [8,9,10]. Enhanced allergic inflammation is found in mice deficient in IL-27 receptor α (IL-27Rα) [11]
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