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The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis
Despite the fact that Candida albicans is an important human fungal pathogen and Dectin-2 is a major pattern recognition receptor for fungi, our knowledge regarding the role of Dectin-2 for the host defense against disseminated candidiasis is limited. Dectin-2 deficient (Dectin-2(−/−)) mice were mor...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mary Ann Liebert, Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4827303/ https://www.ncbi.nlm.nih.gov/pubmed/27046240 http://dx.doi.org/10.1089/jir.2015.0040 |
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author | Ifrim, Daniela C. Quintin, Jessica Courjol, Flavie Verschueren, Ineke van Krieken, J. Han Koentgen, Frank Fradin, Chantal Gow, Neil A.R. Joosten, Leo A.B. van der Meer, Jos W.M. van de Veerdonk, Frank Netea, Mihai G. |
author_facet | Ifrim, Daniela C. Quintin, Jessica Courjol, Flavie Verschueren, Ineke van Krieken, J. Han Koentgen, Frank Fradin, Chantal Gow, Neil A.R. Joosten, Leo A.B. van der Meer, Jos W.M. van de Veerdonk, Frank Netea, Mihai G. |
author_sort | Ifrim, Daniela C. |
collection | PubMed |
description | Despite the fact that Candida albicans is an important human fungal pathogen and Dectin-2 is a major pattern recognition receptor for fungi, our knowledge regarding the role of Dectin-2 for the host defense against disseminated candidiasis is limited. Dectin-2 deficient (Dectin-2(−/−)) mice were more susceptible to systemic candidiasis, and the susceptibility was mirrored by an elevated fungal load in the kidneys that correlated with the presence of large inflammatory foci. Phagocytosis of Candida by the macrophages lacking the Dectin-2 receptor was moderately decreased, while production of most of the macrophage-derived cytokines from Dectin-2(−/−) mice with systemic candidiasis was decreased. No striking differences among several Candida mutants defective in mannans could be detected between naïve wild-type and Dectin-2(−/−) mice, apart from the β-mannan-deficient bmt1Δ/bmt2Δ/bmt5Δ triple mutant, suggesting that β-mannan may partially mask α-mannan detection, which is the major fungal structure recognized by Dectin-2. Deciphering the mechanisms responsible for host defense against the majority of C. albicans strains represents an important step in understanding the pathophysiology of systemic candidiasis, which might lead to the development of novel immunotherapeutic strategies. |
format | Online Article Text |
id | pubmed-4827303 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Mary Ann Liebert, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-48273032016-04-20 The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis Ifrim, Daniela C. Quintin, Jessica Courjol, Flavie Verschueren, Ineke van Krieken, J. Han Koentgen, Frank Fradin, Chantal Gow, Neil A.R. Joosten, Leo A.B. van der Meer, Jos W.M. van de Veerdonk, Frank Netea, Mihai G. J Interferon Cytokine Res Research Reports Despite the fact that Candida albicans is an important human fungal pathogen and Dectin-2 is a major pattern recognition receptor for fungi, our knowledge regarding the role of Dectin-2 for the host defense against disseminated candidiasis is limited. Dectin-2 deficient (Dectin-2(−/−)) mice were more susceptible to systemic candidiasis, and the susceptibility was mirrored by an elevated fungal load in the kidneys that correlated with the presence of large inflammatory foci. Phagocytosis of Candida by the macrophages lacking the Dectin-2 receptor was moderately decreased, while production of most of the macrophage-derived cytokines from Dectin-2(−/−) mice with systemic candidiasis was decreased. No striking differences among several Candida mutants defective in mannans could be detected between naïve wild-type and Dectin-2(−/−) mice, apart from the β-mannan-deficient bmt1Δ/bmt2Δ/bmt5Δ triple mutant, suggesting that β-mannan may partially mask α-mannan detection, which is the major fungal structure recognized by Dectin-2. Deciphering the mechanisms responsible for host defense against the majority of C. albicans strains represents an important step in understanding the pathophysiology of systemic candidiasis, which might lead to the development of novel immunotherapeutic strategies. Mary Ann Liebert, Inc. 2016-04-01 /pmc/articles/PMC4827303/ /pubmed/27046240 http://dx.doi.org/10.1089/jir.2015.0040 Text en © Daniela C. Ifrim et al. 2016; Published by Mary Ann Liebert, Inc. This Open Access article is distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. |
spellingShingle | Research Reports Ifrim, Daniela C. Quintin, Jessica Courjol, Flavie Verschueren, Ineke van Krieken, J. Han Koentgen, Frank Fradin, Chantal Gow, Neil A.R. Joosten, Leo A.B. van der Meer, Jos W.M. van de Veerdonk, Frank Netea, Mihai G. The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis |
title | The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis |
title_full | The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis |
title_fullStr | The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis |
title_full_unstemmed | The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis |
title_short | The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis |
title_sort | role of dectin-2 for host defense against disseminated candidiasis |
topic | Research Reports |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4827303/ https://www.ncbi.nlm.nih.gov/pubmed/27046240 http://dx.doi.org/10.1089/jir.2015.0040 |
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