Abstract

Asthma, atopic dermatitis and chronic rhinoconjunctivitis are highly heterogeneous. However, epidemiologic associations exist between phenotypic groups of patients. Atopic march is one such association but is not the only common point. Indeed, beyond such phenotypes, hallmarks of type 2 immunity have been found in these diseases involving immune dysregulation as well as environmental triggers and epithelial dysfunction. From the canonical Th2 cytokines (IL‐4, IL‐5, IL‐13), new cellular and molecular actors arise, from the epithelium's alarmins to new innate immune cells. Their interactions are now better understood across the different environmental barriers, and slight differences appeared. In parallel, the development of type 2‐targeting biotherapies not only raised hope to treat those diseases but also raised new questions regarding their true pathophysiological involvement. Here, we review the place of type 2 immunity in the different phenotypes of asthma, chronic rhinitis, chronic rhinosinusitis and atopic dermatitis, highlighting nuances between them. New hypotheses rising from the use of biotherapies will be discussed along with the uncertainties and unmet needs of this field.

Highlights

  • Atopic dermatitis (AD), allergic rhinitis (AR), chronic rhinosinusitis with (CRSwNP) or without (CRSsNP) nasal polyps and asthma share a complex interplay between a genetic background, a polarized immune response and the environment

  • In uncontrolled moderate-­ to-­severe AD, dupilumab significantly increased the proportion of patients with an Investigator General Assessment (IGA) score of 0 or 1 or a reduction ≥2 under treatment compared to placebo.[119]

  • Phase 3 clinical trials recently demonstrated a significant improvement of AD under treatment with tralokinumab with or without topical steroids compared with topical steroids alone or placebo.[127,128]

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Summary

Introduction

Atopic dermatitis (AD), allergic rhinitis (AR), chronic rhinosinusitis with (CRSwNP) or without (CRSsNP) nasal polyps and asthma share a complex interplay between a genetic background, a polarized immune response and the environment.

Results
Conclusion
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