Human airway mast cells proliferate and acquire distinct inflammation-driven phenotypes during type 2 inflammation
Daniel F. Dwyer(Brigham and Women's Hospital), José Ordovás-Montañés(Broad Institute), Samuel J. Allon(Broad Institute), Kathleen M. Buchheit(Brigham and Women's Hospital), Marko Vukovic(Broad Institute), Tahereh Derakhshan(Brigham and Women's Hospital), Chunli Feng(Brigham and Women's Hospital), Juying Lai(Brigham and Women's Hospital), Travis K. Hughes(Broad Institute), Sarah K. Nyquist(Broad Institute), Matthew P. Giannetti(Brigham and Women's Hospital), Bonnie Berger(Artificial Intelligence in Medicine (Canada)), Neil Bhattacharyya(Brigham and Women's Hospital), Rachel E. Roditi(Brigham and Women's Hospital), Howard R. Katz(Brigham and Women's Hospital), Martijn C. Nawijn(University Medical Center Groningen), Marijn Berg(University Medical Center Groningen), Maarten van den Berge(University Medical Center Groningen), Tanya M. Laidlaw(Brigham and Women's Hospital), Alex K. Shalek(Broad Institute), Nora A. Barrett(Brigham and Women's Hospital), Joshua A. Boyce(Brigham and Women's Hospital)
Cited by 173Open Access
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.
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