This review summarizes research on mast cells, and the implications of the role and development of mast cells in allergic asthma. The study focuses on the progenitors of mast cells in allergic asthma as well as selected activation pathways and mast cell mediators that have been indicated in pathogenesis. Reviewed data emphasizes describing mechanisms identified using in vivo mouse models and data from analyzed clinical samples.

Allergic asthma is a complex disease with various immune cells, genetic factors, and environmental exposures influencing the pathology. Data has indicated that mast cells play a key role in asthmatic response through the secretion of mediator with pro-inflammatory and airway-constrictive effects. Many of the physiological effects of allergic reactions are triggered by mast cell mediators such as histamines and bioactive lipids. While the accumulation of mast cells at certain sites of allergic lungs could influence asthma phenotype, severity, and progression. The placement of mast cells in different lung compartments and in the airway have different characteristics and express different mediators. Data on in vivo experiments in mice indicate lung mast cells develop from mast cell progenitors that are induced by inflammatory stimuli to migrate to airways. In humans, mast cell progenitors have been found in the blood circulation. This circulation of mast cells could influence continued pathological changes in the allergic lung. While, in allergic asthma, mast cells are activated primarily through IgE-mediated crosslinking of the receptor for IgE with allergens they can also be activated through other stimuli such as toll-like receptors, and MAS-related G protein coupled receptor X2.