Literature DB >> 22580035

The high affinity IgE receptor (FcεRI) expression and function in airway smooth muscle.

Naresh Singh Redhu1, Abdelilah S Gounni.   

Abstract

The airway smooth muscle (ASM) is no longer considered as merely a contractile apparatus and passive recipient of growth factors, neurotransmitters and inflammatory mediators signal but a critical player in the perpetuation and modulation of airway inflammation and remodeling. In recent years, a molecular link between ASM and IgE has been established through Fc epsilon receptors (FcεRs) in modulating the phenotype and function of these cells. Particularly, the expression of high affinity IgE receptor (FcεRI) has been noted in primary human ASM cells in vitro and in vivo within bronchial biopsies of allergic asthmatic subjects. The activation of FcεRI on ASM cells suggests a critical yet almost completely ignored network which may modulate ASM cell function in allergic asthma. This review is intended to provide a historical perspective of IgE effects on ASM and highlights the recent updates in the expression and function of FcεRI, and to present future perspectives of activation of this pathway in ASM cells.
Copyright © 2012 Elsevier Ltd. All rights reserved.

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Year:  2012        PMID: 22580035     DOI: 10.1016/j.pupt.2012.04.004

Source DB:  PubMed          Journal:  Pulm Pharmacol Ther        ISSN: 1094-5539            Impact factor:   3.410


  13 in total

Review 1.  Neuro-Immune Regulation in Inflammation and Airway Remodeling of Allergic Asthma.

Authors:  Ning Zhang; Jing Xu; Congshan Jiang; Shemin Lu
Journal:  Front Immunol       Date:  2022-06-16       Impact factor: 8.786

Review 2.  Is IgE or eosinophils the key player in allergic asthma pathogenesis? Are we asking the right question?

Authors:  Andrea Matucci; Alessandra Vultaggio; Enrico Maggi; Ismail Kasujee
Journal:  Respir Res       Date:  2018-06-08

Review 3.  Evolution of our view on the IgE molecule role in bronchial asthma and the clinical effect of its modulation by omalizumab: Where do we stand today?

Authors:  Jakub Novosad; Irena Krčmová
Journal:  Int J Immunopathol Pharmacol       Date:  2020 Jan-Dec       Impact factor: 3.219

Review 4.  Omalizumab, the first available antibody for biological treatment of severe asthma: more than a decade of real-life effectiveness.

Authors:  Corrado Pelaia; Cecilia Calabrese; Rosa Terracciano; Francesco de Blasio; Alessandro Vatrella; Girolamo Pelaia
Journal:  Ther Adv Respir Dis       Date:  2018 Jan-Dec       Impact factor: 4.031

Review 5.  Targeting Airway Smooth Muscle Hypertrophy in Asthma: An Approach Whose Time Has Come.

Authors:  Anne Chetty; Heber C Nielsen
Journal:  J Asthma Allergy       Date:  2021-05-25

6.  The role of IgE-receptors in IgE-dependent airway smooth muscle cell remodelling.

Authors:  Michael Roth; Jun Zhong; Celine Zumkeller; Chong Teck S'ng; Stephanie Goulet; Michael Tamm
Journal:  PLoS One       Date:  2013-02-14       Impact factor: 3.240

7.  Serum IgE Induced Airway Smooth Muscle Cell Remodeling Is Independent of Allergens and Is Prevented by Omalizumab.

Authors:  Michael Roth; Feng Zhao; Jun Zhong; Didier Lardinois; Michael Tamm
Journal:  PLoS One       Date:  2015-09-02       Impact factor: 3.240

8.  IgE induces proliferation in human airway smooth muscle cells: role of MAPK and STAT3 pathways.

Authors:  Naresh Singh Redhu; Lianyu Shan; Duaa Al-Subait; Heather L Ashdown; Hesam Movassagh; Bouchaib Lamkhioued; Abdelilah S Gounni
Journal:  Allergy Asthma Clin Immunol       Date:  2013-10-17       Impact factor: 3.406

9.  IgE regulates the expression of smMLCK in human airway smooth muscle cells.

Authors:  Jyoti Balhara; Naresh Singh Redhu; Lianyu Shan; Abdelilah S Gounni
Journal:  PLoS One       Date:  2014-04-10       Impact factor: 3.240

Review 10.  Targeted therapy in severe asthma today: focus on immunoglobulin E.

Authors:  Girolamo Pelaia; Giorgio Walter Canonica; Andrea Matucci; Rossella Paolini; Massimo Triggiani; Pierluigi Paggiaro
Journal:  Drug Des Devel Ther       Date:  2017-06-29       Impact factor: 4.162

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