REVIEW: The Role of Interleukin-33 in Pathogenesis of Bronchial Asthma. New Experimental Data

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M. R. Khaitov¹, A. R. Gaisina¹, I. P. Shilovskiy^1*, V. V. Smirnov^1,2, G. V. Ramenskaia², A. A. Nikonova^1,3, and R. M. Khaitov¹

¹Institute of Immunology, FMBA of Russia, 115478 Moscow, Russia; E-mail: ip.shilovsky@nrcii.ru

²Sechenov First Moscow State Medical University, Ministry of Health of the Russian Federation, 119991 Moscow, Russia

³Mechnikov Research Institute for Vaccines and Sera, 105064 Moscow, Russia

^* To whom correspondence should be addressed.

Received May 31, 2017; Revision received September 11, 2017

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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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KEY WORDS: cytokine, interleukin-33, bronchial asthma, mouse model

DOI: 10.1134/S0006297918010029

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