Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

<b>Introduction</b>: Severe asthma is a global health concern with high morbidity and mortality. Understanding of its complex pathophysiology continues to increase, providing specific immune targets for therapeutic intervention.<b>Areas covered</b>: In this review, we focus on the role of IL-4 and IL-13 in severe asthma and on the biologic therapies developed to target them, particularly dupilumab, a monoclonal antibody against the IL-4 receptor α subunit and IL-4/IL-13 receptor complex. A literature search was undertaken for all studies of monoclonal antibodies against IL-4 and IL-13.<b>Expert Opinion</b>: Dupilumab decreases the rate of severe asthma exacerbations and improves symptoms, lung function, and quality of life. Importantly, these effects are also observed during reduction of maintenance oral corticosteroid doses. Those with the highest T2 biomarkers derive the greatest benefit and the presence of atopic dermatitis or chronic rhinosinusitis with or without nasal polyposis may recommend dupilumab as the preferred biologic treatment for a patient.

Original publication

DOI

10.1080/14712598.2020.1714027

Type

Journal article

Journal

Expert opinion on biological therapy

Publication Date

03/2020

Volume

20

Pages

283 - 294

Addresses

Respiratory Medicine Unit and Oxford Respiratory NIHR BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.

Keywords

Humans, Nasopharyngitis, Asthma, Receptors, Interleukin-4, Antibodies, Monoclonal, Treatment Outcome, Half-Life, Receptors, Interleukin-13, Antibodies, Monoclonal, Humanized