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Review
. 2018 Jun 26;11(1):13.
doi: 10.1186/s40413-018-0192-5. eCollection 2018.

Type 2 immunity in asthma

Marco Caminati  1 , Duy Le Pham  2 , Diego Bagnasco  3 , Giorgio Walter Canonica  4
Affiliations
Review

Type 2 immunity in asthma

Marco Caminati et al. World Allergy Organ J. .

Abstract

Type 2-immunity represents the typical adaptive response to allergen exposure in atopic individuals. It mainly involves Th2 cells and immunoglobulin E, as the main orchestrators of type 2-inflammation. Recently, it has been highlighted that allergens may be responsible for a Th2 response beside specific IgE activation and that a number of other environmental stimuli, such as viruses and pollutants, can trigger the same pattern of inflammation beyond atopy. Emerging data sustain a substantial role of the so-called epithelial dysfunction in asthma pathogenesis, both from anatomic and functional point of view. Furthermore an increasing amount of evidence demonstrates the relevance of innate immunity in polarizing a Th2 impaired response in asthmatic patients. Under this perspective, the complex cross-talking between airway epithelium, innate and adaptive immunity is emerging as a major determinant of type 2-inflammation beyond allergens. This review will include an update on the relevance of dysregulation of innate and adaptive type 2-immunity in asthma pathogenesis, particularly severe asthma, and on the role of the allergens that are associated with severe asthma. Type 2-immunity also will be reviewed in the light of the current and upcoming targeted treatments for severe asthma.

Keywords: Adaptive immunity; Allergic sensitization; Asthma; Biologicals; Epithelial dysfunction; Innate immunity; Severe asthma; Type 2 inflammation.

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Conflict of interest statement

Not applicable.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Synthetic overview of asthma Th2 inflammation main determinants. EMT: epithelial-mesenchimal transition; AJC: apical junctional complexes
See this image and copyright information in PMC

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