T-helper cells and their cytokines in the pathogenesis and treatment of asthma

Document Type : Review article


1 Ferdowsi university of Mashhad

2 1Department of Pathobiology, School of Veterinary Medicine, Ferdowsi University of Mashhad, Mashhad, Iran.


Over the past several decades, considerable progress has been made in understanding chronic inflammation and airway remodeling in asthma. Asthma is a chronic inflammatory disease of the airways that causes reversible obstruction of the airways. Asthma symptoms include reversible obstruction of the airways that clear on their own or remit with treatment. "Th2-high" asthma is dominated by eosinophils, sensitive to glucocorticoids, and caused by glucocorticoids. T-helper-2(Th2) immune responses are derived when airway epithelial cells are stimulated by allergens. A series of cytokines are produced first by 2-innate lymphoid cells (ILC2) and then by Th2 cells. These include Interleukin-4(IL-4), Interleukin-5(IL-5), and Interleukin-13(IL-13). Eosinophil inflammation is promoted by IL-5, and IgE production is promoted by IL-13 and IL-4. "Th2-low" asthma is currently defined only as the absence of Th2 inflammation, which may occur in conjunction with other Th cells. It is thought that Th1 and Th17 produce cytokines that are capable of recruiting neutrophils in "Th2-low" asthma. There are several therapeutic approaches involved in the treatment of asthmatic attacks caused by Th cells, as well as a number of potential directions for future research, listed in this review.


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