Abstract
Various cytokines and their receptors implicated in asthma pathophysiology are new targets for future treatments for severe asthma. There are several asthma endotypes that are characterized by the presence of (1) immunoglobulin E (IgE)-mediated inflammation, (2) type 2 inflammation (T2)-high, and (3) T2-low. Endotype-based approaches are new therapeutic strategies for severe asthma. In some countries, monoclonal antibodies (mAbs) that block IgE or interleukin (IL)-5 signaling are being used to treat severe allergic asthma and severe eosinophilic asthma, respectively. Neutralizing mAbs that target the IL-4/IL-13 signaling pathway and thymic stromal lymphopoietin (TSLP) were investigated in several clinical trials involving patients with severe asthma. Drugs generated from these mAbs, such as dupilumab and tezepelumab, may be promising treatments for severe asthma patients. An antagonist of the chemoattractant receptor-homologous molecule on Th2 cells (CRTh2) is another promising drug for the treatment of asthma. Macrolides are also effective for reducing asthma exacerbation in patients with severe asthma. Together, these therapies hold promise for more effective management of asthma.
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