title: Revisiting Type 2-high and Type 2-low airway inflammation in asthma: current knowledge and therapeutic implications.
abstract: 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.
authors.affiliation: Department of Respiratory Medicine, Severe Asthma Service, UCLH NHS Trust, London, UK.
authors.forename: D
authors.identifier: http://orcid.org/0000-0002-0578-740X
authors.initials: D
authors.lastname: Robinson
authors.affiliation: Service de Pneumologie, Hôpital Bicêtre, Assistance Publique Hôpitaux de Paris, University Paris-Sud, Université Paris-Saclay, INSERM U999, Le Kremlin-Bicêtre, France.
authors.forename: M
authors.initials: M
authors.lastname: Humbert
authors.affiliation: Pulmonary Department, Mainz University Hospital, Mainz, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Buhl
authors.affiliation: ProAR-Center of Excellence in Asthma, Federal University of Bahia School of Medicine, Salvador, Brazil.
authors.forename: A A
authors.initials: AA
authors.lastname: Cruz
authors.affiliation: Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Inoue
authors.affiliation: F. Hoffmann-La Roche Ltd, Basel, Switzerland.
authors.forename: S
authors.initials: S
authors.lastname: Korom
authors.affiliation: Section of Pulmonary and Critical Care Medicine, Baylor College of Medicine, Houston, TX, USA.
authors.forename: N A
authors.initials: NA
authors.lastname: Hanania
authors.affiliation: Division of Respirology, Department of Medicine, McMaster University, Hamilton, ON, Canada.
authors.forename: P
authors.identifier: http://orcid.org/0000-0002-1041-9492
authors.initials: P
authors.lastname: Nair
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D015415:Biomarkers; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D018836:Inflammation Mediators / Q000378:metabolism; D015398:Signal Transduction; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators