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The Role of Mast Cells in IgE-Independent Lung Diseases

  • Daniel Elieh Ali Komi
  • , Esmaeil Mortaz
  • , Saeede Amani
  • , Angelica Tiotiu
  • , Gert Folkerts
  • , Ian M. Adcock*
  • *Corresponding author for this work
  • Tabriz University of Medical Sciences
  • Shahid Beheshti University of Medical Sciences
  • Imperial College London

Research output: Contribution to journalReview articlepeer-review

Abstract

Mast cells (MCs) are granular cells of the innate immune system which develop from CD34+/CD117+ progenitors and play a role in orchestrating adaptive immune responses. They have a well-known role in allergic reactions following immunoglobulin (Ig)E-mediated activation of the cell-surface expressed IgE high-affinity receptor (FcεRI). MCs can also respond to various other stimuli due to the expression of a variety of receptors including toll-like receptors (TLRs), immunoglobulin (IgG) receptors (FcγR), complement receptors such as C5a (CD88) expressed by skin MCs, neuropeptides receptors including nerve growth factor receptor, (NGFR), cytokines receptors such as (IL)-1R and IL-3R, and chemokines receptors including CCR-1 and CCR-3. MCs release three groups of mediators upon degranulation differentiated according to their chemical composition, storage, and time to release. These include preformed mediators (mainly histamine, tryptase, and chymase), de novo synthesized mediators such as prostaglandin (PG)D2, leukotriene (LT)B4 and LTD4, and cytokines including IL-1β, IL-3, tumor necrosis factor (TNF)α, and transforming growth factor(TGF)-β. Emerging evidence indicates a role for IgE-independent MC activation in the late-stage asthmatic response as well as in non-allergic airway diseases including chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and lung cancer. MC infiltration/activation has been reported in some, but not all, studies of lung cancer. MC-derived TNF-α possesses tumor-suppressive activity while IL-1β supports tumor progression and metastasis. In IPF lungs, an increase in density of tryptase- and chymase-positive MCs (MCTC) and overexpression of TGF-β support the fibrosis progression. MC-derived chymase activates latent TGF-β that induces the differentiation of fibroblasts to matrix-producing myofibroblasts. In summary, increasing evidence highlights a critical role of MCs in non-allergic diseases that may indicate new approaches for therapy.

Original languageEnglish
Pages (from-to)377–387
JournalClinical Reviews in Allergy and Immunology
Volume58
Early online date21 Feb 2020
DOIs
Publication statusPublished - 2020

Funding

IMA is financially supported by the British Heart Foundation (PG/14/27/30679), Dunhill Medical Trust (R368/0714), Welcome Trust (093080/Z/10/Z), EPSRC (EP/T003189/1), and by the UK MRC (MR/T010371/1). EM is financially supported by NIMAD (982810) and INSF (98003666).

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Antigen-independent
  • COPD
  • IPF
  • Lung cancer
  • Mast cells
  • Non-IgE mast cell activation

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