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dc.contributor.authorBruserud, Øyvinden_US
dc.contributor.authorBratland, Eiriken_US
dc.contributor.authorHellesen, Alexanderen_US
dc.contributor.authorDelaleu, Nicolasen_US
dc.contributor.authorReikvam, Håkonen_US
dc.contributor.authorOftedal, Bergithe Eikelanden_US
dc.contributor.authorWolff, Anette Susanne Bøeen_US
dc.date.accessioned2018-08-06T13:06:07Z
dc.date.available2018-08-06T13:06:07Z
dc.date.issued2017-09-01
dc.PublishedBruserud Ø, Bratland E, Hellesen A, Delaleu N, Reikvam H, Oftedal BE, Wolff AS. Altered immune activation and IL-23 signaling in response to Candida albicans in autoimmune polyendocrine syndrome type 1. Frontiers in Immunology. 2017;8:1074eng
dc.identifier.issn1664-3224
dc.identifier.urihttps://hdl.handle.net/1956/17998
dc.description.abstractObjective: Autoimmune polyendocrine syndrome type 1 (APS-1) is a rare, childhood onset disease caused by mutations in the autoimmune regulator (AIRE) gene. Chronic mucocutaneous candidiasis (CMC) is one of the three major disease components and is, to date, mainly explained by the presence of neutralizing auto-antibodies against cytokines [interleukin (IL)-17A, IL-17F, and IL-22] from T helper 17 cells, which are critical for the protection against fungal infections. However, patients without current auto-antibodies also present CMC and we, therefore, hypothesized that other immune mechanisms contribute to CMC in APS-1. Methods: Whole blood was stimulated with Candida albicans (C. albicans) in a standardized assay, and immune activation was investigated by analyzing 46 secreted immune mediators. Then, peripheral blood mononuclear cells were stimulated with curdlan, a Dectin-1 agonist and IL-23 inducer, and the IL-23p19 response in monocytes was analyzed by flow cytometry. Results: We found an altered immune response in APS-1 patients compared with healthy controls. Patients fail to increase the essential ILs, such as IL-2, IL-17A, IL-22, and IL-23, when stimulating whole blood with C. albicans. A significantly altered IL-23p19 response was detected in patients’ monocytes upon stimulation with curdlan. Conclusion: APS-1 patients have an altered immune response to C. albicans including a dysregulation of IL-23p19 production in monocytes. This probably contributes to the selective susceptibility to CMC found in the majority of patients.en_US
dc.language.isoengeng
dc.publisherFrontierseng
dc.rightsAttribution CC BYeng
dc.rights.urihttp://creativecommons.org/licenses/by/4.0eng
dc.subjectautoimmune polyendocrine syndrome type 1eng
dc.subjectchronic mucocutaneous candidiasiseng
dc.subjectmonocyteseng
dc.subjectIL-17eng
dc.subjectIL-22eng
dc.subjectIL-23eng
dc.titleAltered immune activation and IL-23 signaling in response to Candida albicans in autoimmune polyendocrine syndrome type 1en_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2018-03-06T12:58:12Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2017 The Author(s)
dc.identifier.doihttps://doi.org/10.3389/fimmu.2017.01074
dc.identifier.cristin1512724
dc.source.journalFrontiers in Immunology


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