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Innate Immune Responses in House Dust Mite Allergy

Sensitizations to house dust mites (HDM) trigger strong exacerbated allergen-induced inflammation of the skin and airways mucosa from atopic subjects resulting in atopic dermatitis as well as allergic rhinitis and asthma. Initially, the Th2-biased HDM allergic response was considered to be mediated...

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Detalles Bibliográficos
Autor principal: Jacquet, Alain
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658386/
https://www.ncbi.nlm.nih.gov/pubmed/23724247
http://dx.doi.org/10.1155/2013/735031
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author Jacquet, Alain
author_facet Jacquet, Alain
author_sort Jacquet, Alain
collection PubMed
description Sensitizations to house dust mites (HDM) trigger strong exacerbated allergen-induced inflammation of the skin and airways mucosa from atopic subjects resulting in atopic dermatitis as well as allergic rhinitis and asthma. Initially, the Th2-biased HDM allergic response was considered to be mediated only by allergen B- and T-cell epitopes to promote allergen-specific IgE production as well as IL-4, IL-5, and IL-13 to recruit inflammatory cells. But this general molecular model of HDM allergenicity must be revisited as a growing literature suggests that stimulations of innate immune activation pathways by HDM allergens offer new answers to the following question: what makes an HDM allergen an allergen? Indeed, HDM is a carrier not only for allergenic proteins but also microbial adjuvant compounds, both of which are able to stimulate innate signaling pathways leading to allergy. This paper will describe the multiple ways used by HDM allergens together with microbial compounds to control the initiation of the allergic response through engagement of innate immunity.
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spelling pubmed-36583862013-05-30 Innate Immune Responses in House Dust Mite Allergy Jacquet, Alain ISRN Allergy Review Article Sensitizations to house dust mites (HDM) trigger strong exacerbated allergen-induced inflammation of the skin and airways mucosa from atopic subjects resulting in atopic dermatitis as well as allergic rhinitis and asthma. Initially, the Th2-biased HDM allergic response was considered to be mediated only by allergen B- and T-cell epitopes to promote allergen-specific IgE production as well as IL-4, IL-5, and IL-13 to recruit inflammatory cells. But this general molecular model of HDM allergenicity must be revisited as a growing literature suggests that stimulations of innate immune activation pathways by HDM allergens offer new answers to the following question: what makes an HDM allergen an allergen? Indeed, HDM is a carrier not only for allergenic proteins but also microbial adjuvant compounds, both of which are able to stimulate innate signaling pathways leading to allergy. This paper will describe the multiple ways used by HDM allergens together with microbial compounds to control the initiation of the allergic response through engagement of innate immunity. Hindawi Publishing Corporation 2013-02-28 /pmc/articles/PMC3658386/ /pubmed/23724247 http://dx.doi.org/10.1155/2013/735031 Text en Copyright © 2013 Alain Jacquet. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Jacquet, Alain
Innate Immune Responses in House Dust Mite Allergy
title Innate Immune Responses in House Dust Mite Allergy
title_full Innate Immune Responses in House Dust Mite Allergy
title_fullStr Innate Immune Responses in House Dust Mite Allergy
title_full_unstemmed Innate Immune Responses in House Dust Mite Allergy
title_short Innate Immune Responses in House Dust Mite Allergy
title_sort innate immune responses in house dust mite allergy
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658386/
https://www.ncbi.nlm.nih.gov/pubmed/23724247
http://dx.doi.org/10.1155/2013/735031
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