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Mechanisms of pathogenesis in allergic asthma: Role of interleukin‐23
Author(s) -
Li Yanchun,
Hua Shucheng
Publication year - 2014
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/resp.12299
Subject(s) - medicine , immunology , asthma , eosinophil , pathogenesis , cytokine , inflammation , interleukin 13 , allergy , interleukin
Asthma is a chronic airway inflammatory disease characterized by intense leukocyte and eosinophilic infiltration accompanied by mucus hypersecretion and tissue hyperresponsiveness. Recent evidence suggests that T ‐helper ( T h)2 cells and their cytokine products orchestrate the pathology of asthma. In addition, T h17 cells are implicated in the pathogenesis of antigen‐induced airway inflammation. The T h17 related cytokine interleukin ( IL )‐23 plays important roles in many immunological diseases, such as experimental autoimmune encephalomyelitis, rheumatoid arthritis, psoriasis and inflammatory bowel disease. Several reports describe the role of IL ‐23 in the pathogenesis of allergic asthma in both human and mice. IL ‐23 leads to neutrophil infiltration in the airway of asthmatic mice, which is characteristic of severe asthma resulting from T h17 development and subsequently IL ‐17 secretion. IL ‐23 can also promote eosinophil infiltration in the airway, which is a hallmark of allergic asthma. These studies suggest that IL ‐23 could be a promoting factor in the development of allergic asthma and likewise would be a target for asthma therapy. In support of this view, trials of anti‐ IL ‐23 therapy have been attempted in human and mouse asthma models with encouraging outcomes. This review presents the role of IL ‐23 in asthma according to recent clinical trials and animal model studies. The proposed mechanisms of IL ‐23‐induced airway inflammation and the agents currently being tested that target IL ‐23 related pathways are discussed.