IL-23, rather than IL-17, is crucial for the development of ovalbumin-induced allergic rhinitis

被引:13
作者
Guo, Chaobin [1 ]
Chen, Guie [2 ]
Ge, Ruifeng [3 ]
机构
[1] Qingdao Municiple Hosp, Qingdao 266000, Peoples R China
[2] Third Peoples Hosp Qingdao, Qingdao 66041, Peoples R China
[3] Qingdao Univ, Affiliated Hosp, Qingdao 266003, Peoples R China
关键词
Allergic rhinitis; IL-23; IL-17; Eosinophil; TH17; CELLS; T-CELLS; SERUM INTERLEUKIN-17; AIRWAY INFLAMMATION; ASTHMA; EXPRESSION; CANCER; MULTICENTER; POPULATION; PATHOLOGY;
D O I
10.1016/j.molimm.2015.07.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Interleukin-23 (IL-23) and IL-17 are involved in the pathogenesis of allergic rhinitis (AR). However, the roles of IL-23 and IL-17 in ovalbumin (OVA)-induced AR remain unclear. Therefore in this study we aim to investigate the precise roles of IL-23 and IL-17 in a mouse model of OVA-induced AR. We found that during OVA-induced AR, eosinophil and goblet cells in the nose were significantly decreased in IL-23-deficient, but not in IL-17-deficient mice. However, there was no difference in the serum IgE and IgG1 levels between IL-23-deficient or IL-17-deficient and wild-type mice. Moreover, IL-4 levels in lymph node cell culture supernatants were significantly decreased in IL-23-deficient, but not IL-17-deficient, compared with wild-type mice. Furthermore, OVA-induced AR developed similarly in wild-type mice transferred with either IL-23-deficient BM cells or wild-type BM cells. These findings suggest that IL-23, but not IL-17 is crucial for the development of OVA-induced AR, and IL-23 neutralization may be a potential approach for treatment of OVA-induced AR in humans. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:436 / 443
页数:8
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