Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348143
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampPedroza, Luis Alberto-
dc.typeArtigopt_BR
dc.titleAutoimmune regulator (AIRE) contributes to dectin-1–induced TNF-α production and complexes with caspase recruitment domain–containing protein 9 (CARD9), spleen tyrosine kinase (Syk), and dectin-1pt_BR
dc.contributor.authorPedroza, Luis A.-
dc.contributor.authorKumar, Vipul-
dc.contributor.authorSanborn, Keri B.-
dc.contributor.authorMace, Emily M.-
dc.contributor.authorNiinikoski, Harri-
dc.contributor.authorNadeau, Kari-
dc.contributor.authorVasconcelos, Dewton de Moraes-
dc.contributor.authorPerez, Elena-
dc.contributor.authorJyonouchi, Soma-
dc.contributor.authorJyonouchi, Harumi-
dc.contributor.authorBanerjee, Pinaki P.-
dc.contributor.authorRuuskanen, Olli-
dc.contributor.authorCondino-Neto, Antonio-
dc.contributor.authorOrange, Jordan S.-
dc.subjectImunidade naturalpt_BR
dc.subject.otherlanguageNatural immunitypt_BR
dc.description.abstractAutoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECED) syndrome is a complex immunologic disease caused by mutation of the autoimmune regulator (AIRE) gene. Autoimmunity in patients with APECED syndrome has been shown to result from deficiency of AIRE function in transcriptional regulation of thymic peripheral tissue antigens, which leads to defective T-cell negative selection. Candidal susceptibility in patients with APECED syndrome is thought to result from aberrant adaptive immunity. To determine whether AIRE could function in anticandidal innate immune signaling, we investigated an extrathymic role for AIRE in the immune recognition of β-glucan through the Dectin-1 pathway, which is required for defense against Candida species. Innate immune signaling through the Dectin-1 pathway was assessed in both PBMCs from patients with APECED syndrome and a monocytic cell line. Subcellular localization of AIRE was assessed by using confocal microscopy. PBMCs from patients with APECED syndrome had reduced TNF-α responses after Dectin-1 ligation but in part used a Raf-1–mediated pathway to preserve function. In the THP-1 human monocytic cell line, reducing AIRE expression resulted in significantly decreased TNF-α release after Dectin-1 ligation. AIRE formed a transient complex with the known Dectin-1 pathway components phosphorylated spleen tyrosine kinase and caspase recruitment domain–containing protein 9 after receptor ligation and localized with Dectin-1 at the cell membrane. AIRE can participate in the Dectin-1 signaling pathway, indicating a novel extrathymic role for AIRE and a defect that likely contributes to fungal susceptibility in patients with APECED syndromept_BR
dc.relation.ispartofJournal of allergy and clinical immunologypt_BR
dc.relation.ispartofabbreviationJ. allergy clin. immunol.pt_BR
dc.publisher.cityPhiladelphia, PApt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherElsevierpt_BR
dc.date.issued2012-
dc.date.monthofcirculationFeb.pt_BR
dc.language.isoengpt_BR
dc.description.volume129pt_BR
dc.description.issuenumber2pt_BR
dc.description.firstpage464pt_BR
dc.description.lastpage472pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0091-6749pt_BR
dc.identifier.eissn1097-6825pt_BR
dc.identifier.doi10.1016/j.jaci.2011.08.027pt_BR
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0091674911013935pt_BR
dc.date.available2020-08-27T16:54:21Z-
dc.date.accessioned2020-08-27T16:54:21Z-
dc.description.provenanceSubmitted by Mariana Aparecida Azevedo (mary1@unicamp.br) on 2020-08-27T16:54:21Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:14:25Z : No. of bitstreams: 1 000299951700026.pdf: 1458914 bytes, checksum: 47b96067891fe3d78bfa96e9871f40d4 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-08-27T16:54:21Z (GMT). No. of bitstreams: 0 Previous issue date: 2012en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348143-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.subject.keywordPrimary immunodeficiencypt_BR
dc.subject.keywordChronic mucocutaneouspt_BR
dc.subject.keywordCandidiasispt_BR
dc.subject.keywordMonocytespt_BR
dc.identifier.source000299951700026pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.type.formArtigopt_BR
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