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Increased IL-17A secretion in response to Candida albicans in autoimmune polyendocrine syndrome type 1 and its animal model

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dc.contributor.authorAhlgren, K.
dc.contributor.authorMoretti, S.
dc.contributor.authorLundgren, B.
dc.contributor.authorKarlsson, I.
dc.contributor.authorAhlin, E.
dc.contributor.authorNorling, A.
dc.contributor.authorHallgren, A.
dc.contributor.authorPerheentupa, J.
dc.contributor.authorGustafsson, J.
dc.contributor.authorRorsman, F.
dc.contributor.authorCrewther, P.
dc.contributor.authorRonnelid, J.
dc.contributor.authorBensing, S.
dc.contributor.authorScott, H.
dc.contributor.authorKampe, O.
dc.contributor.authorRomani, L.
dc.contributor.authorLobell, A.
dc.date.issued2011
dc.descriptionData source: Supporting information, https://doi.org/10.1002/eji.200939883 Link to a related website: https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/eji.200939883, Open Access via Unpaywall
dc.description.abstractAutoimmune polyendocrine syndrome type 1 (APS-1) is a multiorgan autoimmune disease caused by mutations in the autoimmune regulator (AIRE) gene. Chronic mucocutaneous candidiasis, hypoparathyroidism and adrenal failure are hallmarks of the disease. The critical mechanisms causing chronic mucocutaneous candidiasis in APS-1 patients have not been identified although autoantibodies to cytokines are implicated in the pathogenesis. To investigate whether the Th reactivity to Candida albicans (C. albicans) and other stimuli was altered, we isolated PBMC from APS-1 patients and matched healthy controls. The Th17 pathway was upregulated in response to C. albicans in APS-1 patients, whereas the IL-22 secretion was reduced. Autoantibodies against IL-22, IL-17A and IL-17F were detected in sera from APS-1 patients by immunoprecipitation. In addition, Aire-deficient (Aire 0/0 ) mice were much more susceptible than Aire +/+ mice to mucosal candidiasis and C. albicans-induced Th17- and Th1-cell responses were increased in Aire 0/0 mice. Thus an excessive IL-17A reactivity towards C. albicans was observed in APS-1 patients and Aire 0/0 mice.
dc.description.statementofresponsibilityKerstin M. Ahlgren, Silvia Moretti, Brita Ardesjö Lundgren, Iulia Karlsson, Erik Åhlin, Anna Norling, Åsa Hallgren, Jaakko Perheentupa, Jan Gustafsson, Fredrik Rorsman, Pauline E. Crewther, Johan Rönnelid, Sophie Bensing, Hamish S. Scott, Olle Kämpe, Luigina Romani and Anna Lobell
dc.identifier.citationEuropean Journal of Immunology, 2011; 41(1):235-245
dc.identifier.doi10.1002/eji.200939883
dc.identifier.issn0014-2980
dc.identifier.issn1521-4141
dc.identifier.orcidScott, H. [0000-0002-5813-631X]
dc.identifier.urihttp://hdl.handle.net/2440/62959
dc.language.isoen
dc.publisherWiley-V C H Verlag GMBH
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/171601
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/461204
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/257501
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/264573
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/406700
dc.rightsCopyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
dc.source.urihttps://doi.org/10.1002/eji.200939883
dc.subjectAutoimmunity
dc.subjectCytokines
dc.subjectFungal
dc.subjectT cells
dc.titleIncreased IL-17A secretion in response to Candida albicans in autoimmune polyendocrine syndrome type 1 and its animal model
dc.typeJournal article
pubs.publication-statusPublished

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