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Revisiting Type 2‐high and Type 2‐low airway inflammation in asthma: current knowledge and therapeutic implications

Robinson, D., Humbert, M., Buhl, R., Cruz, A. A., Inoue, H., Korom, S., Hanania, N. A., Nair, P.·2017·Clinical & Experimental Allergy

Abstract

Summary: Asthma is a complex respiratory disorder characterized by marked heterogeneity in individual patient disease triggers and response to therapy. Several asthma phenotypes have now been identified, each defined by a unique interaction between genetic and environmental factors, including inflammatory, clinical and trigger‐related phenotypes. Endotypes further describe the functional or pathophysiologic mechanisms underlying the patient's disease. type 2‐driven asthma is an emerging nomenclature for a common subtype of asthma and is characterized by the release of signature cytokines IL ‐4, IL ‐5 and IL ‐13 from cells of both the innate and adaptive immune systems. A number of well‐recognized biomarkers have been linked to mechanisms involved in type 2 airway inflammation, including fractional exhaled nitric oxide, serum IgE, periostin, and blood and sputum eosinophils. These type 2 cytokines are targets for pharmaceutical intervention, and a number of therapeutic options are under clinical investigation for the management of patients with uncontrolled severe asthma. Anticipating and understanding the heterogeneity of asthma and subsequent improved characterization of different phenotypes and endotypes must guide the selection of treatment to meet individual patients’ needs.

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Fig. 1 Overview of a type 2-driven asthma response: type 2 cytokines drive the recruitment of effector cells (e.g. eosinophils) and mediate class switching of B cells to secrete IgE upon exposure to antigens. They are also central to many of the hallmarks of asthma, including mucus production, subepithelial fibrosis, bronchial remodelling and airway hyperresponsiveness.
Fig. 1 Overview of a type 2-driven asthma response: type 2 cytokines drive the recruitment of effector cells (e.g. eosinophils) and mediate class switching of B cells to secrete IgE upon exposure to antigens. They are also central to many of the hallmarks of asthma, including mucus production, subepithelial fibrosis, bronchial remodelling and airway hyperresponsiveness.CC-BY-NC · From the PDF

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Metadata

Authors
Robinson, D., Humbert, M., Buhl, R., Cruz, A. A., Inoue, H., Korom, S., Hanania, N. A., & Nair, P.
Affiliations
  • Department of Respiratory Medicine Severe Asthma Service UCLH NHS Trust London UK
  • Service de Pneumologie Hôpital Bicêtre Assistance Publique Hôpitaux de Paris University Paris‐Sud Université Paris‐Saclay INSERM U999 Le Kremlin‐Bicêtre France
  • Pulmonary Department Mainz University Hospital Mainz Germany
  • ProAR‐Center of Excellence in Asthma Federal University of Bahia School of Medicine Salvador Brazil
  • Department of Pulmonary Medicine Graduate School of Medical and Dental Sciences Kagoshima University Kagoshima Japan
  • F. Hoffmann‐La Roche Ltd Basel Switzerland
  • Section of Pulmonary and Critical Care Medicine Baylor College of Medicine Houston TX USA
  • Division of Respirology Department of Medicine McMaster University Hamilton ON Canada
Venue
Clinical & Experimental Allergy
Publisher
Wiley
Published
2017-01-30
Volume
47
Issue
2
Pages
161-175
ISSN
  • 0954-7894
  • 1365-2222
Cited by
357
References
5
Language
en
Funders
  • AstraZeneca
  • Chiesi Farmaceutici
  • Roche
  • Teva Pharmaceutical Industries
  • Boehringer Ingelheim
  • GlaxoSmithKline
  • Novartis
  • Merck Sharp and Dohme
  • Astellas Pharma US
  • Pfizer
  • Sanofi

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