IL-13 mediates IL-33–dependent mast cell and type 2 innate lymphoid cell effects on bronchial epithelial cells Deepti R. Nagarkar, PhD, Vladimir Ramirez-Carrozzi, PhD, David F. Choy, BS, Kevin Lee, BSc, Robert Soriano, BA, Guiquan Jia, MD, Alexander R. Abbas, PhD, Zora Modrusan, PhD, Rajita Pappu, PhD, Joseph R. Arron, MD, PhD Journal of Allergy and Clinical Immunology Volume 136, Issue 1, Pages 202-205 (July 2015) DOI: 10.1016/j.jaci.2015.01.036 Copyright © 2015 American Academy of Allergy, Asthma & Immunology Terms and Conditions
Fig 1 IL-33–stimulated mast cells activate IL-13–regulated gene expression in NHBE cells (A-C and G). NHBE cells stimulated as indicated alone or in coculture with mast cells for 72 hours. IL-13 was blocked with anti–IL-13 or isotype control. N = 5-6, ILC2 activated NHBE cells gene expression (D-F and H) for 72 hours. Differential gene expression is abrogated on the addition of anti–IL-13 antibody (N = 3). Results are shown as mean ± SD fold change compared with respective medium control. CLCA1, Calcium-activated chloride channel regulator-1.*P < .05, paired Student t test. Journal of Allergy and Clinical Immunology 2015 136, 202-205DOI: (10.1016/j.jaci.2015.01.036) Copyright © 2015 American Academy of Allergy, Asthma & Immunology Terms and Conditions