ABSTRACT
Allergic rhinitis (AR) is a noninfectious inflammatory response in nasal mucosa caused by allergens, which is contacted by a specific individual. The immune imbalance of Th1/Th2 plays an important role in the pathogenesis of AR. In?terleukin (IL)-33, the novel cytokine of IL-1 family, is an important regulatory factor of allergic diseases, autoimmune diseas?es and various inflammatory diseases. IL-33 is a kind of alarm, which is mainly secreted and released by damaged tissues and cells, especially impaired epithelial cells and endothelial cells. IL-33 binding to its receptor ST2L can activate a variety of immune cells to produce Th2 cytokines, precipitating and maintaining Th2 polarization, increasing AR immune inflamma?tion, which is the new target of AR in research and treatment. In this article, we have done a brief overview for the biological functions of IL-33 and its receptor ST2L and the research progress in the AR.
ABSTRACT
The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 +/- 464.0 pg/mL) than in healthy controls (96.0 +/- 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1beta (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naive RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA.