Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Immunol. Nov 27, 2016; 6(3): 126-130
Published online Nov 27, 2016. doi: 10.5411/wji.v6.i3.126
IgE regulates airway smooth muscle phenotype: Future perspectives in allergic asthma
Naresh Singh Redhu, Abdelilah S Gounni
Naresh Singh Redhu, Division of GI/Nutrition, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, United States
Abdelilah S Gounni, Department of Immunology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB R3E0T5, Canada
Author contributions: Redhu NS and Gounni AS conceptualized, drafted, and revised the full manuscript.
Conflict-of-interest statement: None.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Abdelilah S Gounni, PhD, Professor, Department of Immunology, Faculty of Health Sciences, College of Medicine, University of Manitoba, 419 Apotex Centre, 750 McDermot Ave, Winnipeg, MB R3E0T5, Canada. abdel.gounni@umanitoba.ca
Telephone: +1-204-9757750 Fax: +1-204-7893921
Received: May 21, 2016
Peer-review started: May 22, 2016
First decision: July 30, 2016
Revised: August 15, 2016
Accepted: October 25, 2016
Article in press: October 27, 2016
Published online: November 27, 2016
Core Tip

Core tip: In this commentary, we summarize the emerging role IgE in influencing airway smooth (ASM) muscle function in allergic asthma. Recent intriguing findings from ours and other groups suggest a potential proinflammatory and pro-remodeling role of IgE-mediated activation of its high-affinity Fc receptor, i.e., FcεRI, on ASM tissue in allergic asthma.