Abstract

The complex pathogenesis of atopic eczema involves an impaired epidermal barrier, dysbiosis, and aberrant type 2 immunity (Eyerich and Eyerich, 2018; Werfel et al., 2015) depending on cytokines such as IL-4, IL-5, IL-9, IL-13, and IL-31 as well as eosinophils, basophils, mast cells, and IgE (Eyerich and Eyerich, 2018). This is underpinned by the clinical efficacy of novel therapeutic targets interacting with type 2 immunity such as the IL-4Ra antibody dupilumab (Blauvelt et al., 2017).

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.