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 (Th)2 cells and their
cytokine products orchestrate the pathology of
asthma. In addition, Th17 cells are implicated in the pathogenesis of
antigen-induced airway
inflammation. The Th17 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 Th17 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.