title: The TH2-polarizing function of atopic interleukin 17 receptor B-positive dendritic cells up-regulated by lipopolysaccharide.
abstract: Recent studies suggest that epithelial cell (EC)-derived cytokines contribute to allergic airway disease exacerbation.
  
  
  
  To confirm our hypothesis that atopic dendritic cells (DCs) are activated to up-regulate the receptors of cytokines that mainly derived from ECs and enhance TH2 responses.
  
  
  
  The expressions of interleukin 17 receptor B (IL-17RB) (IL-25 receptor), membrane-bound ST2 (IL-33 receptor), thymic stromal lymphopoietin receptor (TSLPR), granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR), and several functional markers on CD1c+monocyte-derived DCs (mo-DCs) were detected by flow cytometry. Lipopolysaccharide (LPS)-activated mo-DCs were cocultured with autologous CD4+T cells, and cytokine production by these T cells was determined by intracellular flow cytometry.
  
  
  
  LPS activated both nonatopic and atopic mo-DCs to express a higher level of GM-CSFR but only activated atopic mo-DCs to express increased IL-17RB, which was subsequently activated by IL-25 involved with signal transducer and activator of transcription 5 phosphorylation. In addition, LPS increased the expression of the OX40 ligand (OX40L) but decreased inducible costimulator ligand on atopic CD86+mo-DCs. More importantly, IL-25 further up-regulated OX40L on atopic CD86+mo-DCs. After coculturing with LPS-activated mo-DCs from atopic individuals, CD4+T cells had enhanced inflammatory responses by increased production of IL-4, IL-5, IL-13, and interferon γ (IFN-γ). In contrast, further addition of IL-25 led CD4+T cells to produce higher level of IL-4 but lower level of IFN-γ.
  
  
  
  Atopic IL-17RB+DCs can be up-regulated by LPS and promote a TH2-type response, implying that the IL-25/IL-17RB pathway may represent a potential molecular mechanism underlying the regulation of ECs on DCs in allergic airway disease.
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Zheng
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Feng-Hong
authors.initials: FH
authors.lastname: Chen
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Wen-Xiang
authors.initials: WX
authors.lastname: Gao
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Wang
authors.affiliation: Department of Otorhinolaryngology-Head and Neck Surgery, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Qin-Tai
authors.initials: QT
authors.lastname: Yang
authors.affiliation: Department of Otorhinolaryngology-Head and Neck Surgery, First People's Hospital of Foshan, Foshan, Guangdong, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Wang
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Yin-Yan
authors.initials: YY
authors.lastname: Lai
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Deng
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Li-Jie
authors.initials: LJ
authors.lastname: Jiang
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Yue-Qi
authors.initials: YQ
authors.lastname: Sun
authors.affiliation: Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China. Electronic address: tsjbent@163.com.
authors.forename: Jian-Bo
authors.initials: JB
authors.lastname: Shi
mesh_terms: D000328:Adult; D000485:Allergens; D015415:Biomarkers; D016022:Case-Control Studies; D016207:Cytokines / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism*; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology* / Q000378:metabolism*; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D016130:Immunophenotyping; D008070:Lipopolysaccharides / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D009000:Monocytes / Q000276:immunology / Q000378:metabolism; D053722:Receptors, Interleukin-17 / Q000378:metabolism*; D020545:Respiratory Mucosa / Q000276:immunology / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism; D055815:Young Adult
chemical_list: D000485:Allergens; D015415:Biomarkers; D016207:Cytokines; D008070:Lipopolysaccharides; D053722:Receptors, Interleukin-17; D007073:Immunoglobulin E