Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2021:2270:375-418.
doi: 10.1007/978-1-0716-1237-8_21.

Regulatory and IgE+ B Cells in Allergic Asthma

Affiliations

Regulatory and IgE+ B Cells in Allergic Asthma

John Paul Oliveria et al. Methods Mol Biol. 2021.

Abstract

Allergic asthma is triggered by inhalation of environmental allergens resulting in bronchial constriction and inflammation, which leads to clinical symptoms such as wheezing, coughing, and difficulty breathing. Asthmatic airway inflammation is initiated by inflammatory mediators released by granulocytic cells. However, the immunoglobulin E (IgE) antibody is necessary for the initiation of the allergic cascade, and IgE is produced and released exclusively by memory B cells and plasma cells. Acute allergen exposure has also been shown to increase IgE levels in the airways of patients diagnosed with allergic asthma; however, more studies are needed to understand local airway inflammation. Additionally, regulatory B cells (Bregs) have been shown to modulate IgE-mediated inflammatory processes in allergic asthma pathogenesis, particularly in mouse models of allergic airway disease. However, the levels and function of these IgE+ B cells and Bregs remain to be elucidated in human models of asthma. The overall objective for this chapter is to provide detailed methodological, and insightful technological advances to study the biology of B cells in allergic asthma pathogenesis. Specifically, we will describe how to investigate the frequency and function of IgE+ B cells and Bregs in allergic asthma, and the kinetics of these cells after allergen exposure in a human asthma model.

Keywords: Airway inflammation; Allergic asthma; Human immunology; IgE+ B cells; Inhaled allergen challenge; Regulatory B cells; Sputum.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Lotvall J, Akdis CA, Barcharier LB, Bjermer L, Casale TB, Custovic A, Lemanske RF Jr, Wardlaw AJ, Wenzel SE, Greenberger PA (2015) Asthma endotypes: a new approach to classification of disease entities within the asthma syndrome. J Allergy Clin Immunol 127(2):355–360. https://doi.org/10.1016/j.jaci.2010.11.037 - DOI
    1. Akdis CA, Akdis M (2015) Mechanisms of allergen-specific immunotherapy and immune tolerance to allergens. World Allergy Organization Journal 8(1):17–17. https://doi.org/10.1186/s40413-015-0063-2 - DOI
    1. Wills-Karp M (1999) Immunologic basis of antigen-induced airway hyperresponsiveness. Annu Rev Immunol 17(1):255–281. https://doi.org/10.1146/annurev.immunol.17.1.255 - DOI - PubMed
    1. Wills-Karp M (2004) Interleukin-13 in asthma pathogenesis. Immunol Rev 202(1):175–190. https://doi.org/10.1111/j.0105-2896.2004.00215.x - DOI - PubMed
    1. Gauvreau GM, Evans MY (2007) Allergen inhalation challenge: a human model of asthma exacerbation. Contrib Microbiol 14:21–32. https://doi.org/10.1159/0000107052 - DOI - PubMed

Publication types

Grants and funding

LinkOut - more resources