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Mechanisms of immune tolerance to allergens: role of IL-10 and Tregs
Cezmi A. Akdis, Mübeccel Akdis
Cezmi A. Akdis, Mübeccel Akdis
Published November 3, 2014
Citation Information: J Clin Invest. 2014;124(11):4678-4680. https://doi.org/10.1172/JCI78891.
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Mechanisms of immune tolerance to allergens: role of IL-10 and Tregs

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Abstract

During the past 20 years, major advances have been made in understanding the molecular and cellular mechanisms of allergen tolerance in humans. The demonstration of T cell tolerance, particularly that mediated by the immune-suppressive functions of IL-10, led to a major conceptual change in this area. Currently, the known essential components of allergen tolerance include the induction of allergen-specific regulatory subsets of T and B cells, the immune-suppressive function of secreted factors, such as IL-10 and TGF-β, the production of IgG4 isotype allergen–specific blocking antibodies, and decreased allergic inflammatory responses by mast cells, basophils, and eosinophils in inflamed tissues.

Authors

Cezmi A. Akdis, Mübeccel Akdis

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Figure 1

Mechanisms of allergen tolerance.

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Mechanisms of allergen tolerance.
The induction of allergen-specific Tre...
The induction of allergen-specific Tregs, which switch from allergen-specific Th2 cells is one of the initial events in the development of allergen tolerance. The effector cells of allergic inflammation — mast cells, basophils, and eosinophils — are regulated by suppressive and regulatory functions of Tregs in several ways. Treg-secreted IL-10 and TGF-β suppress these cells. Tregs also suppress Th2 cells and their cytokines, preventing the provision of survival factors for these allergy effector cells. IL-10 and TGF-β suppress IgE production by B cells, and meanwhile, IL-10 induces IgG4. IL-10–producing regulatory B cells (Bregs) play a role in suppression of allergen-specific T cells and mainly switch to IgG4-producing plasma cells. H2R plays a role in the suppression of Th2 cells, inflammatory dendritic cells, and basophils.

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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