TY - JOUR
T1 - Diagnosis and Management of T2-High Asthma
AU - Coverstone, Andrea M.
AU - Seibold, Max A.
AU - Peters, Michael C.
N1 - Funding Information:
Conflicts of interest: A. M. Coverstone reports no relevant conflicts of interest. M. A. Seibold reports grants from the National Institutes of Health, Medimmune, Genentech, and the Department of Defense, during the conduct of the study; grants from Pfizer and AstraZeneca, outside the submitted work; patent inventions “Methods of identifying and treating subjects having inflammatory subphenotypes on asthma” (in process: File No. 2879-178-PROV pending), “Transcriptomic response of airway epithelial cells to IL-13” (in process: File No. 2879-190-PROV-1 pending), and “Methods of diagnosing and treating subjects at risk of inflammation and/or exacerbation of a respiratory disease or condition” (in process: File No. 2879-191-PROV-1 pending); and delivering an invited lecture for Genentech. M. C. Peters reports personal fees from Merck; and grants from AstraZeneca, Boehringer-Ingelheim, Genentech, GlaxoSmithKline, Sanofi-Genzyme-Regeneron, and TEVA, outside the submitted work.
Funding Information:
>Conflicts of interest: A. M. Coverstone reports no relevant conflicts of interest. M. A. Seibold reports grants from the National Institutes of Health, Medimmune, Genentech, and the Department of Defense, during the conduct of the study; grants from Pfizer and AstraZeneca, outside the submitted work; patent inventions ?Methods of identifying and treating subjects having inflammatory subphenotypes on asthma? (in process: File No. 2879-178-PROV pending), ?Transcriptomic response of airway epithelial cells to IL-13? (in process: File No. 2879-190-PROV-1 pending), and ?Methods of diagnosing and treating subjects at risk of inflammation and/or exacerbation of a respiratory disease or condition? (in process: File No. 2879-191-PROV-1 pending); and delivering an invited lecture for Genentech. M. C. Peters reports personal fees from Merck; and grants from AstraZeneca, Boehringer-Ingelheim, Genentech, GlaxoSmithKline, Sanofi-Genzyme-Regeneron, and TEVA, outside the submitted work.
Publisher Copyright:
© 2019
PY - 2020/2
Y1 - 2020/2
N2 - Type 2 (T2) inflammation plays a key role in the pathogenesis of asthma. IL-4, IL-5, and IL-13, along with other inflammatory mediators, lead to increased cellular eosinophilic inflammation. It is likely that around half of all patients with asthma have evidence of T2-high inflammation. Sputum and blood eosinophils, exhaled nitric oxide, blood IgE levels, and airway gene expression markers are frequently used biomarkers of T2-high asthma. Individuals with T2-high asthma tend to have several features of increased asthma severity, including reduced lung function and increased rates of asthma exacerbations, and T2-high patients demonstrate distinct pathologic features including increased airway remodeling and alterations in airway mucus production. Several monoclonal antibodies are now available to treat individuals with T2-high asthma and these medications significantly reduce asthma exacerbation rates.
AB - Type 2 (T2) inflammation plays a key role in the pathogenesis of asthma. IL-4, IL-5, and IL-13, along with other inflammatory mediators, lead to increased cellular eosinophilic inflammation. It is likely that around half of all patients with asthma have evidence of T2-high inflammation. Sputum and blood eosinophils, exhaled nitric oxide, blood IgE levels, and airway gene expression markers are frequently used biomarkers of T2-high asthma. Individuals with T2-high asthma tend to have several features of increased asthma severity, including reduced lung function and increased rates of asthma exacerbations, and T2-high patients demonstrate distinct pathologic features including increased airway remodeling and alterations in airway mucus production. Several monoclonal antibodies are now available to treat individuals with T2-high asthma and these medications significantly reduce asthma exacerbation rates.
KW - Asthma
KW - Biomarkers in asthma
KW - Monoclonal antibody therapy
KW - Type 2 inflammation
UR - http://www.scopus.com/inward/record.url?scp=85078314308&partnerID=8YFLogxK
U2 - 10.1016/j.jaip.2019.11.020
DO - 10.1016/j.jaip.2019.11.020
M3 - Article
C2 - 32037108
AN - SCOPUS:85078314308
SN - 2213-2198
VL - 8
SP - 442
EP - 450
JO - Journal of Allergy and Clinical Immunology: In Practice
JF - Journal of Allergy and Clinical Immunology: In Practice
IS - 2
ER -