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Cholera toxin B suppresses allergic inflammation through induction of secretory IgA

H. Smits, A. Gloudemans, M. van Nimwegen, Monique Willart, T. Soullié, F. Muskens, E. de Jong, L. Boon, C. Pilette, F.-E. Johansen, et al. (2009) Mucosal Immunology. 2(4). p.331-339
abstract
In healthy individuals, humoral immune responses to allergens consist of serum IgA and IgG4, whereas cellular immune responses are controlled by regulatory T (Treg) cells. In search of new compounds that might prevent the onset of allergies by stimulating this type of immune response, we have focused on the mucosal adjuvant, cholera toxin B (CTB), as it induces the formation of Treg cells and production of IgA. Here, we have found that CTB suppresses the potential of dendritic cells to prime for Th2 responses to inhaled allergen. When we administered CTB to the airways of naive and allergic mice, it strongly suppressed the salient features of asthma, such as airway eosinophilia, Th2 cytokine synthesis, and bronchial hyperreactivity. This beneficial effect was only transferable to other mice by transfer of B but not of T lymphocytes. CTB caused a transforming growth factor-beta-dependent rise in antigen-specific IgA in the airway luminal secretions, which was necessary for its preventive and curative effect, as all effects of CTB were abrogated in mice lacking the luminal IgA transporting polymeric Ig receptor. Not only do these findings show a novel therapeutic avenue for allergy, they also help to explain the complex relationship between IgA levels and risk of developing allergy in humans.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
delivery-system, subunit, inhaled antigen, immuneresponses, tolerance induction, regulatory T-cells, dendritic cells, asthma, challenge, adjuvant
journal title
Mucosal Immunology
Mucosal Immunol.
volume
2
issue
4
pages
331 - 339
publisher
Nature Publishing Group
place of publication
New York
Web of Science type
Article
Web of Science id
000267055000008
JCR category
IMMUNOLOGY
JCR impact factor
3.627 (2009)
JCR rank
35/126 (2009)
JCR quartile
2 (2009)
ISSN
1933-0219
DOI
10.1038/mi.2009.16
language
English
UGent publication?
yes
classification
A1
id
798046
handle
http://hdl.handle.net/1854/LU-798046
date created
2009-12-02 16:07:23
date last changed
2017-01-02 09:56:07
@article{798046,
  abstract     = {In healthy individuals, humoral immune responses to allergens consist of serum IgA and IgG4, whereas cellular immune responses are controlled by regulatory T (Treg) cells. In search of new compounds that might prevent the onset of allergies by stimulating this type of immune response, we have focused on the mucosal adjuvant, cholera toxin B (CTB), as it induces the formation of Treg cells and production of IgA. Here, we have found that CTB suppresses the potential of dendritic cells to prime for Th2 responses to inhaled allergen. When we administered CTB to the airways of naive and allergic mice, it strongly suppressed the salient features of asthma, such as airway eosinophilia, Th2 cytokine synthesis, and bronchial hyperreactivity. This beneficial effect was only transferable to other mice by transfer of B but not of T lymphocytes. CTB caused a transforming growth factor-beta-dependent rise in antigen-specific IgA in the airway luminal secretions, which was necessary for its preventive and curative effect, as all effects of CTB were abrogated in mice lacking the luminal IgA transporting polymeric Ig receptor. Not only do these findings show a novel therapeutic avenue for allergy, they also help to explain the complex relationship between IgA levels and risk of developing allergy in humans.},
  author       = {Smits, H. and Gloudemans, A. and van Nimwegen, M. and Willart, Monique and Soulli{\'e}, T. and Muskens, F. and de Jong, E. and Boon, L. and Pilette, C. and Johansen, F.-E. and Hoogsteden, H. and Hammad, Hamida and Lambrecht, Bart},
  issn         = {1933-0219},
  journal      = {Mucosal Immunology},
  keyword      = {delivery-system,subunit,inhaled antigen,immuneresponses,tolerance induction,regulatory T-cells,dendritic cells,asthma,challenge,adjuvant},
  language     = {eng},
  number       = {4},
  pages        = {331--339},
  publisher    = {Nature Publishing Group},
  title        = {Cholera toxin B suppresses allergic inflammation through induction of secretory IgA},
  url          = {http://dx.doi.org/10.1038/mi.2009.16},
  volume       = {2},
  year         = {2009},
}

Chicago
Smits, H., A. Gloudemans, M. van Nimwegen, Monique Willart, T. Soullié, F. Muskens, E. de Jong, et al. 2009. “Cholera Toxin B Suppresses Allergic Inflammation Through Induction of Secretory IgA.” Mucosal Immunology 2 (4): 331–339.
APA
Smits, H., Gloudemans, A., van Nimwegen, M., Willart, M., Soullié, T., Muskens, F., de Jong, E., et al. (2009). Cholera toxin B suppresses allergic inflammation through induction of secretory IgA. Mucosal Immunology, 2(4), 331–339.
Vancouver
1.
Smits H, Gloudemans A, van Nimwegen M, Willart M, Soullié T, Muskens F, et al. Cholera toxin B suppresses allergic inflammation through induction of secretory IgA. Mucosal Immunology. New York: Nature Publishing Group; 2009;2(4):331–9.
MLA
Smits, H., A. Gloudemans, M. van Nimwegen, et al. “Cholera Toxin B Suppresses Allergic Inflammation Through Induction of Secretory IgA.” Mucosal Immunology 2.4 (2009): 331–339. Print.