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The role of interleukin-33 in pathogenesis of bronchial asthma. New experimental data
Authors:M. R. Khaitov  A. R. Gaisina  I. P. Shilovskiy  V. V. Smirnov  G. V. Ramenskaia  A. A. Nikonova  R. M. Khaitov
Affiliation:1.Institute of Immunology,FMBA of Russia,Moscow,Russia;2.Sechenov First Moscow State Medical University, Ministry of Health of the Russian Federation,Moscow,Russia;3.Mechnikov Research Institute for Vaccines and Sera,Moscow,Russia
Abstract:Interleukin-33 (IL-33) belongs to the IL-1 cytokine family and plays an important role in modulating immune system by inducing Th2 immune response via the ST2 membrane receptor. Epithelial cells are the major producers of IL-33. However, IL-33 is also secreted by other cells, e.g., bone marrow cells, dendritic cells, macrophages, and mast cells. IL-33 targets a broad range of cell types bearing the ST2 surface receptor. Many ST2-positive cells, such as Th2 cells, mast cells, basophils, and eosinophils, are involved in the development of allergic bronchial asthma (BA). This suggests that IL-33 directly participates in BA pathogenesis. Currently, the role of IL-33 in pathogenesis of inflammatory disorders, including BA, has been extensively investigated using clinical samples collected from patients, as well as asthma animal models. In particular, numerous studies on blocking IL-33 and its receptor by monoclonal antibodies in asthma mouse model have been performed over the last several years; IL-33-and ST2-deficient transgenic mice have also been generated. In this review, we summarized and analyzed the data on the role of IL-33 in BA pathogenesis and the prospects for creating new treatments for BA.
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