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B Cells Play Key Roles in Th2-Type Airway Immune Responses in Mice Exposed to Natural Airborne Allergens
Humans are frequently exposed to various airborne allergens. In addition to producing antibodies, B cells participate in immune responses via various mechanisms. The roles of B cells in allergic airway inflammation and asthma have been controversial. We examined the functional importance of B cells...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4372217/ https://www.ncbi.nlm.nih.gov/pubmed/25803300 http://dx.doi.org/10.1371/journal.pone.0121660 |
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author | Drake, Li Yin Iijima, Koji Hara, Kenichiro Kobayashi, Takao Kephart, Gail M. Kita, Hirohito |
author_facet | Drake, Li Yin Iijima, Koji Hara, Kenichiro Kobayashi, Takao Kephart, Gail M. Kita, Hirohito |
author_sort | Drake, Li Yin |
collection | PubMed |
description | Humans are frequently exposed to various airborne allergens. In addition to producing antibodies, B cells participate in immune responses via various mechanisms. The roles of B cells in allergic airway inflammation and asthma have been controversial. We examined the functional importance of B cells in a mouse model of asthma, in which mice were exposed repeatedly to common airborne allergens. Naïve wild-type BALB/c mice or B cell-deficient JH(−/−) mice were exposed intranasally to a cocktail of allergen extracts, including Alternaria, Aspergillus, and house dust mite, every other day for two weeks. Ovalbumin was included in the cocktail to monitor the T cell immune response. Airway inflammation, lung pathology, and airway reactivity were analyzed. The airway exposure of naïve wild type mice to airborne allergens induced robust eosinophilic airway inflammation, increased the levels of Th2 cytokines and chemokines in the lung, and increased the reactivity to inhaled methacholine. These pathological changes and immune responses were attenuated in B cell-deficient JH(−/−) mice. The allergen-induced expansion of CD4(+) T cells was impaired in the lungs and draining lymph nodes of JH(−/−) mice. Furthermore, lymphocytes from JH(−/−) mice failed to produce Th2 cytokines in response to ovalbumin re-stimulation in vitro. Our results suggest that B cells are required for the optimal development of Th2-type immune responses and airway inflammation when exposed to common airborne allergens. The therapeutic targeting of B cells may be beneficial to treat asthma in certain patients. |
format | Online Article Text |
id | pubmed-4372217 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-43722172015-04-04 B Cells Play Key Roles in Th2-Type Airway Immune Responses in Mice Exposed to Natural Airborne Allergens Drake, Li Yin Iijima, Koji Hara, Kenichiro Kobayashi, Takao Kephart, Gail M. Kita, Hirohito PLoS One Research Article Humans are frequently exposed to various airborne allergens. In addition to producing antibodies, B cells participate in immune responses via various mechanisms. The roles of B cells in allergic airway inflammation and asthma have been controversial. We examined the functional importance of B cells in a mouse model of asthma, in which mice were exposed repeatedly to common airborne allergens. Naïve wild-type BALB/c mice or B cell-deficient JH(−/−) mice were exposed intranasally to a cocktail of allergen extracts, including Alternaria, Aspergillus, and house dust mite, every other day for two weeks. Ovalbumin was included in the cocktail to monitor the T cell immune response. Airway inflammation, lung pathology, and airway reactivity were analyzed. The airway exposure of naïve wild type mice to airborne allergens induced robust eosinophilic airway inflammation, increased the levels of Th2 cytokines and chemokines in the lung, and increased the reactivity to inhaled methacholine. These pathological changes and immune responses were attenuated in B cell-deficient JH(−/−) mice. The allergen-induced expansion of CD4(+) T cells was impaired in the lungs and draining lymph nodes of JH(−/−) mice. Furthermore, lymphocytes from JH(−/−) mice failed to produce Th2 cytokines in response to ovalbumin re-stimulation in vitro. Our results suggest that B cells are required for the optimal development of Th2-type immune responses and airway inflammation when exposed to common airborne allergens. The therapeutic targeting of B cells may be beneficial to treat asthma in certain patients. Public Library of Science 2015-03-24 /pmc/articles/PMC4372217/ /pubmed/25803300 http://dx.doi.org/10.1371/journal.pone.0121660 Text en © 2015 Drake et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Drake, Li Yin Iijima, Koji Hara, Kenichiro Kobayashi, Takao Kephart, Gail M. Kita, Hirohito B Cells Play Key Roles in Th2-Type Airway Immune Responses in Mice Exposed to Natural Airborne Allergens |
title | B Cells Play Key Roles in Th2-Type Airway Immune Responses in Mice Exposed to Natural Airborne Allergens |
title_full | B Cells Play Key Roles in Th2-Type Airway Immune Responses in Mice Exposed to Natural Airborne Allergens |
title_fullStr | B Cells Play Key Roles in Th2-Type Airway Immune Responses in Mice Exposed to Natural Airborne Allergens |
title_full_unstemmed | B Cells Play Key Roles in Th2-Type Airway Immune Responses in Mice Exposed to Natural Airborne Allergens |
title_short | B Cells Play Key Roles in Th2-Type Airway Immune Responses in Mice Exposed to Natural Airborne Allergens |
title_sort | b cells play key roles in th2-type airway immune responses in mice exposed to natural airborne allergens |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4372217/ https://www.ncbi.nlm.nih.gov/pubmed/25803300 http://dx.doi.org/10.1371/journal.pone.0121660 |
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