title: Autoimmune Regulator Expression in DC2.4 Cells Regulates the NF-κB Signaling and Cytokine Expression of the Toll-Like Receptor 3 Pathway.
abstract: Autoimmune regulator (Aire) mutations result in autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED), which manifests as multi-organ autoimmunity and chronic mucocutaneous candidiasis (CMC). Indendritic cells (DCs), pattern recognition receptors (PRR), such as Toll-like receptors (TLRs), are closely involved in the recognition of various pathogens, activating the intercellular signaling pathway, followed by the activation of transcription factors and the expression of downstream genes, which take part in mediating the immune response and maintaining immune tolerance. In this study, we found that Aire up-regulated TLR3 expression and modulated the downstream cytokine expression and nuclear factor-κB (NF-κB) of the TLR3 signaling pathway.
authors.affiliation: Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China. sjitong@163.com.
authors.forename: Jitong
authors.initials: J
authors.lastname: Sun
authors.affiliation: Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China. niukw123@163.com.
authors.forename: Kunwei
authors.initials: K
authors.lastname: Niu
authors.affiliation: Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China. fuhy@jlu.edu.cn.
authors.forename: Haiying
authors.initials: H
authors.lastname: Fu
authors.affiliation: Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China. lidongbei2008@163.com.
authors.forename: Haijun
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China. liyi@jlu.edu.cn.
authors.forename: Yi
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China. ywei@jlu.edu.cn.
authors.forename: Wei
authors.initials: W
authors.lastname: Yang
mesh_terms: D000818:Animals; D015551:Autoimmunity / Q000235:genetics / Q000276:immunology; D002175:Candida / Q000276:immunology / Q000472:pathogenicity; D002178:Candidiasis, Chronic Mucocutaneous / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation; D006801:Humans; D007108:Immune Tolerance / Q000235:genetics; D051379:Mice; D009154:Mutation; D016328:NF-kappa B / Q000235:genetics; D016884:Polyendocrinopathies, Autoimmune / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D051196:Toll-Like Receptor 3 / Q000096:biosynthesis* / Q000276:immunology; D014157:Transcription Factors / Q000096:biosynthesis* / Q000235:genetics; D000096927:AIRE Protein
chemical_list: D016328:NF-kappa B; D051196:Toll-Like Receptor 3; D014157:Transcription Factors; D000096927:AIRE Protein; C519703:TLR3 protein, mouse
keywords: TLR3; autoimmune regulator; immune tolerance