Fig. 1
Asthma, a chronic inflammatory airway disease, is characterized by eosinophilic inflammation, mucus hypersecretion, goblet cell hyperplasia, airway hyper-responsiveness, and breathlessness. Th2 cell immune responses are dominant in the pathophysiology of asthma. IL-4, IL-5, and IL-13 are released by Th2 cells. IL-4 has a role in B-cell IgE isotype switching and upregulation of FcεRI on mast cells, which release histamine and other mediators that lead to allergic symptoms and smooth muscle spasm. IL-5 leads to activation, migration, and accumulation of eosinophils to the airway and initiates bronchial inflammation. IL-13 has a main role in mucus hypersecretion and goblet cell hyperplasia and promotes AHR. Therefore, a focus on the mechanisms of cell signaling that are related to asthma for designing new drugs and targeted molecules can be continued with the aforementioned parameters
