[Advances in the mechanism and research of epithelial-derived alarmins in driving allergic diseases].

Abstract

Allergen-associated proteases, pollutants, viral and fungal pathogens disrupted epithelial barrier integrity and promoted airway epithelial release of alarmins.Epithelial-derived Alarmins include thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25), which acted on a variety of effector cells such as dendritic cells (DCs), T-lymphocytes, innate lymphocyte cells (ILC2), B-lymphocytes, eosinophils, mast cells, basophils, and macrophages. T-lymphocytes, innate lymphocyte cell type 2 (ILC2), B-lymphocytes, eosinophils, mast cells, basophils and macrophages are the effector cells. By affecting the physiological and biochemical functions of target cells, such as proliferation and differentiation, survival and recruitment, and material metabolism, the alarmins had activated the intrinsic and adaptive immunity, and played a key role in allergic diseases such as bronchial asthma, atopic dermatitis, allergic rhinitis, and urticaria. A variety of monoclonal antibodies targeting epithelial-derived alarm factors have been developed for the above allergic diseases, and some of these products are already put into clinical use. As epidemiological studies showed that skin allergy closely related to airway allergy, allergic co-morbidities has imposed a heavy economic and psychological burden to patients. In-depth understanding the mechanism of alarmins will help to understand the developing and progression of allergic diseases, and develop more effective diagnostic and therapeutic strategies for allergic co-morbidities. This article reviews the mechanism and recent research advances of epithelial-derived alarmins in a variety of allergic diseases.