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Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice
BACKGROUND: Epicutaneous sensitization with protein allergen that induces predominant Th2 responses is an important sensitization route in atopic dermatitis. Fungal components have been shown to modulate Th cell differentiation. However, the effects of fungal components on epicutaneous sensitization...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563454/ https://www.ncbi.nlm.nih.gov/pubmed/23286586 http://dx.doi.org/10.1186/1423-0127-20-1 |
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author | Lin, Jing-Yi Chen, Jau-Shiuh Chen, Pei-Chun Chung, Ming-Hui Liu, Ching-Yi Miaw, Shi-Chuen Wang, Li-Fang |
author_facet | Lin, Jing-Yi Chen, Jau-Shiuh Chen, Pei-Chun Chung, Ming-Hui Liu, Ching-Yi Miaw, Shi-Chuen Wang, Li-Fang |
author_sort | Lin, Jing-Yi |
collection | PubMed |
description | BACKGROUND: Epicutaneous sensitization with protein allergen that induces predominant Th2 responses is an important sensitization route in atopic dermatitis. Fungal components have been shown to modulate Th cell differentiation. However, the effects of fungal components on epicutaneous sensitization are unclear. RESULTS: In this study, we showed that co-administration of curdlan, a dectin-1 agonist, during epicutaneous ovalbumin sensitization of BALB/c mice decreased the IL-5 and IL-13 levels in supernatants of lymph node cell ovalbumin reactivation cultures. Mechanistically, curdlan co-administration decreased IL-4 and IL-1β expressions in draining lymph nodes. Curdlan co-administration also lower the migration of langerin(+) CD103(-) epidermal Langerhans cells into draining lymph nodes at 96 hours post-sensitization which might be attributed to decreased expressions of IL-18 and IL-1β in patched skin. Moreover, adoptive transfer of CFSE-labeled transgenic CD4 T cells confirmed that curdlan co-administration decreased the proliferation and IL-4-production of ovalbumin -specific T cells primed by epidermal Langerhans cells. CONCLUSIONS: These results indicated that concurrent exposure to a dectin-1 agonist suppresses the epicutaneously induced Th2 response by modulating the cytokine expression profiles in draining LNs and the migration of epidermal Langerhans cells. These results highlight the effects of fungal components on epicutaneous allergen sensitization in atopic diseases. |
format | Online Article Text |
id | pubmed-3563454 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-35634542013-02-08 Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice Lin, Jing-Yi Chen, Jau-Shiuh Chen, Pei-Chun Chung, Ming-Hui Liu, Ching-Yi Miaw, Shi-Chuen Wang, Li-Fang J Biomed Sci Research BACKGROUND: Epicutaneous sensitization with protein allergen that induces predominant Th2 responses is an important sensitization route in atopic dermatitis. Fungal components have been shown to modulate Th cell differentiation. However, the effects of fungal components on epicutaneous sensitization are unclear. RESULTS: In this study, we showed that co-administration of curdlan, a dectin-1 agonist, during epicutaneous ovalbumin sensitization of BALB/c mice decreased the IL-5 and IL-13 levels in supernatants of lymph node cell ovalbumin reactivation cultures. Mechanistically, curdlan co-administration decreased IL-4 and IL-1β expressions in draining lymph nodes. Curdlan co-administration also lower the migration of langerin(+) CD103(-) epidermal Langerhans cells into draining lymph nodes at 96 hours post-sensitization which might be attributed to decreased expressions of IL-18 and IL-1β in patched skin. Moreover, adoptive transfer of CFSE-labeled transgenic CD4 T cells confirmed that curdlan co-administration decreased the proliferation and IL-4-production of ovalbumin -specific T cells primed by epidermal Langerhans cells. CONCLUSIONS: These results indicated that concurrent exposure to a dectin-1 agonist suppresses the epicutaneously induced Th2 response by modulating the cytokine expression profiles in draining LNs and the migration of epidermal Langerhans cells. These results highlight the effects of fungal components on epicutaneous allergen sensitization in atopic diseases. BioMed Central 2013-01-03 /pmc/articles/PMC3563454/ /pubmed/23286586 http://dx.doi.org/10.1186/1423-0127-20-1 Text en Copyright ©2013 Lin et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Lin, Jing-Yi Chen, Jau-Shiuh Chen, Pei-Chun Chung, Ming-Hui Liu, Ching-Yi Miaw, Shi-Chuen Wang, Li-Fang Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice |
title | Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice |
title_full | Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice |
title_fullStr | Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice |
title_full_unstemmed | Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice |
title_short | Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice |
title_sort | concurrent exposure to a dectin-1 agonist suppresses the th2 response to epicutaneously introduced antigen in mice |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563454/ https://www.ncbi.nlm.nih.gov/pubmed/23286586 http://dx.doi.org/10.1186/1423-0127-20-1 |
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