title: Porphyromonas gingivalis fimbriae induce unique dendritic cell subsets via Toll-like receptor 2.
abstract: OBJECTIVE
  Dendritic cells (DCs) play a critical role in the activation of T cells as well as in shaping immune responses. We have reported previously that Porphyromonas gingivalis lipopolysaccharides (Pg LPS) induced a CD14(+)CD16(+) DC subset with a weak immuno-stimulatory activity. In contrast, Escherichia coli LPS (Ec LPS) induced fully matured DCs with strong immunostimulatory activities. Since Pg LPS as well as Pg fimbriae have been indicated to work as Toll-like receptor (TLR) 2 ligands, we speculate that the TLR usage of bacterial antigens may be critical for DC maturation.
  
  
  METHODS
  We investigated the effect of Pg fimbriae on the phenotype and function of human peripheral blood DCs in comparison with a TLR2 ligand, peptidoglycan, and a TLR4 ligand, Ec LPS.
  
  
  RESULTS
  Flow cytometry revealed that Pg fimbriae and peptidoglycan but not Ec LPS induced CD14 and CD16 expression on peripheral blood DCs (CD14(-)CD16(-)). A monoclonal antibody against TLR2 abrogated this induction, but an antibody against TLR4 had no effect. Dendritic cells stimulated with Pg fimbriae had a weaker capability to induce allogenic T cell proliferation and exhibited a weaker production of interleukin-8 and regulated upon activation, normal T cell expressed and secreted (RANTES) than DCs stimulated with Ec LPS.
  
  
  CONCLUSIONS
  These results indicate that different TLR usage affects mature DC phenotype and function and is thus crucial to the regulation of immunity to the pathogen.
authors.affiliation: Division of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry, Sendai, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Kanaya
authors.forename: E
authors.initials: E
authors.lastname: Nemoto
authors.forename: T
authors.initials: T
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Shimauchi
mesh_terms: D049109:Cell Proliferation; D018946:Chemokine CCL5 / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology*; D004926:Escherichia coli / Q000276:immunology; D010861:Fimbriae, Bacterial / Q000276:immunology*; D005434:Flow Cytometry; D006801:Humans; D016209:Interleukin-8 / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D010457:Peptidoglycan / Q000276:immunology; D010641:Phenotype; D016966:Porphyromonas gingivalis / Q000276:immunology*; D017452:Receptors, IgG / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D051195:Toll-Like Receptor 2 / Q000276:immunology*; D051197:Toll-Like Receptor 4 / Q000276:immunology
chemical_list: C483024:CCL5 protein, human; D018946:Chemokine CCL5; D016209:Interleukin-8; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D010457:Peptidoglycan; D017452:Receptors, IgG; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4