Abstract
For the last decade, the attention of researchers has been attracted by Toll-like receptors that provide recognition of pathogens and trigger an immune response to them. As participants in acute infectious processes, with inadequate stimulation associated with mutation of genes regulating expression of the receptors, they cause the initiation or exacerbation of asthma in predisposed individuals. At the same time, the reduced function of the receptors leads to an insufficient immune response in respiratory infectious diseases, which also leads to an exacerbation of bronchial asthma. In addition, Toll-like receptors are direct elements of the pathogenesis of bronchial asthma, supporting or reducing inflammation. Thus, Toll-like receptors can not only aggravate the course of asthma, but also prevent exacerbations of the disease. Knowledge of the role of these receptors in the pathophysiology of bronchial asthma is necessary to improve diagnostic methods and timely detection of the disease. Using data on the effects realized by the receptors, medicines are being developed that are antagonists or agonists of a Toll-like receptors. The use of medicines acting on receptors in the treatment and prevention of asthma in the future may lead to increased control over the course of the disease.
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