Insights into mast cell hyperplasia in aspirin-exacerbated respiratory disease from transcriptional profiling of polyp mast cells

Abstract

Asthma is a complex, heterogeneous lung disease arising from the interaction of genetic, environmental, and immunologic factors. An emerging feature of asthma across multiple disease endotypes is the expansion of mast cells (MCs), tissue-resident granulocytes that are believed to participate in disease progression, in the airway smooth muscle, bronchial epithelium, and alveolar parenchyma.1 Of note, 2 main subsets of human MCs have been described, both of which expand during asthma: MCTC that contain the proteases tryptase and chymase and mainly reside in peripheral connective tissues and MCT that contain tryptase in the absence of chymase and reside within the epithelium.