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Inhaled corticosteroid responses in COPD: do mast cells hold the answer?
  1. Andrew Higham1,
  2. Dave Singh1,2
  1. 1 Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester University NHS Foundation Trust, Manchester, UK
  2. 2 Medicines Evaluation Unit, Manchester, UK
  1. Correspondence to Professor Dave Singh, Medicines Evaluation Unit, Manchester University NHS Foundation Trust, University of Manchester, Manchester, M23 9QZ, Greater Manchester, UK; dsingh{at}

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Mast cells provide innate immune defence against microbes through the secretion of various mediators including proteases, with mucosal-like and connective tissue-like mast cells being tryptase+chymase- (MCT) and tryptase+chymase+ (MCTC), respectively. Mast cells are found in high numbers in the lungs, with MCT being predominant in the airways.1 2 Mast cells also participate in adaptive immune responses by Fc receptor-mediated antibody recognition.3 The multifunctional capabilities of mast cells can turn against the host to cause disease, such as IgE-mediated degranulation in allergy and asthma.3

Inhaled corticosteroids (ICSs) reduce exacerbation rates in patients with chronic obstructive pulmonary disease (COPD) with a history of exacerbations.4 5 Patients with COPD with higher eosinophil counts, measured in sputum or blood, are more likely to benefit from ICS treatment, with blood eosinophil counts (BEC) now used in clinical practice to aid patient selection for treatment.4 5 Increased BEC reflect higher pulmonary eosinophil counts6 7 and a broader milieu of pulmonary type-2 (T2) inflammation in COPD including the T2 cytokines IL-5 and IL-13.7–9 Importantly, the profile of T2 inflammation in COPD differs from asthma.8 9 ICSs do not reduce lung eosinophil numbers,10 11 suggesting that other T2 components are the targets of ICS in COPD.

In this issue, Faiz et al further investigate T2 inflammation …

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  • Contributors Both authors contributed equally to this work.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests DS has acted as a consultant for Aerogen, AstraZeneca, Boehringer Ingelheim, Chiesi, Cipla, CSL Behring, EpiEndo, Genentech, GlaxoSmithKline, Glenmark, Gossamer Bio, Kinaset Therapeutics, Menarini, Novartis, Orion, Pulmatrix, Sanofi, Teva, Theravance Biopharma and Verona Pharma.

  • Provenance and peer review Commissioned; externally peer reviewed.

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