Human airway mast cells proliferate and acquire distinct inflammation-driven phenotypes during type 2 inflammation
Daniel F. Dwyer, José Ordovás-Montañés, Samuel J. Allon, Kathleen M. Buchheit, Marko Vukovic, Tahereh Derakhshan, Chunli Feng, Juying Lai, Travis K. Hughes, Sarah K. Nyquist, Matthew P. Giannetti, Bonnie Berger, Neil Bhattacharyya, Rachel E. Roditi, Howard R. Katz, Martijn C. Nawijn, Marijn Berg, Maarten van den Berge, Tanya M. Laidlaw, Alex K. Shalek, Nora A. Barrett, Joshua A. Boyce
Abstract
in nasal polyps and skin. These results indicate that MCs display distinct inflammation-associated effector programs and suggest that in situ MC proliferation is a major component of MC hyperplasia in human T2 inflammation.
Topics & Concepts
InflammationPhenotypeImmunologyBiologyMast cellAllergic inflammationMast (botany)Cell biologyGeneticsGeneMast cells and histamineAsthma and respiratory diseasesIL-33, ST2, and ILC Pathways