title: IL-23-producing CD68(+) macrophage-like cells predominate within an IL-17-polarized infiltrate in chronic periodontitis lesions.
abstract: OBJECTIVE
  To analyse antigen-presenting cells (APCs), such as dendritic cells (DCs), macrophages (Mo) or B cells depending on the regional site of chronic periodontitis (CP), and to investigate their relation to Th17 cells.
  
  
  METHODS
  Biopsies from oral mucosa as well as the coronal and bottom regions of CP were analysed by immunhistochemistry, immunofluorescence, flow cytometry and real-time PCR.
  
  
  RESULTS
  A predominance of CD68(+) Mo-like cells and CD20(+) B cells and strong Th17 infiltration was observed in the bottom region of CP lesions, while CD1a(+) DCs were only detected in the coronal regions, where Th17 infiltration was low. Furthermore, CD68(+) Mo-like cells displayed CD163 expression as a typical Mo-marker, but expressed in parallel typical DCs markers, such as CD11c or CD209 and TLR4. Interestingly, Th17-inducing cytokine IL-23p19 was produced by CD68(+) Mo-like cells, but not CD20(+) B cells. Moreover, the stimulation of in vitro generated CD68(+) Mo-like cells by Porphyromonas gingivalis-derived (Pg) lipopolysaccharide resulted in the upregulation of their IL-23p19 mRNA expression, which was inhibited by the blockage of TLR4.
  
  
  CONCLUSIONS
  In view of these data, a picture emerges that IL-17-producing cells in CP could be in part directed by CD68(+) Mo-like cells, which produce IL-23p19 upon TLR4 activation by Pg.
authors: Department of Dermatology and Allergy, University of Bonn, Germany.
authors: Jean-Pierre
authors: JP
authors: Allam
authors: Yonggang
authors: Y
authors: Duan
authors: Friedhelm
authors: F
authors: Heinemann
authors: Jochen
authors: J
authors: Winter
authors: Werner
authors: W
authors: Götz
authors: James
authors: J
authors: Deschner
authors: Matthias
authors: M
authors: Wenghoefer
authors: Thomas
authors: T
authors: Bieber
authors: Soren
authors: S
authors: Jepsen
authors: Natalija
authors: N
authors: Novak
mesh_terms: D000368:Aged; D000938:Antigen-Presenting Cells / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D015703:Antigens, CD / Q000276:immunology; D018951:Antigens, CD20 / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology; D055113:Chronic Periodontitis / Q000276:immunology* / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology; D053759:Interleukin-23 / Q000096:biosynthesis*; D053760:Interleukin-23 Subunit p19 / Q000276:immunology; D008070:Lipopolysaccharides; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009061:Mouth Mucosa / Q000276:immunology / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000276:immunology; D060888:Real-Time Polymerase Chain Reaction; D058504:Th17 Cells / Q000276:immunology*; D051197:Toll-Like Receptor 4 / Q000502:physiology; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D018951:Antigens, CD20; D015214:Antigens, Differentiation, Myelomonocytic; D020381:Interleukin-17; D053759:Interleukin-23; D053760:Interleukin-23 Subunit p19; D008070:Lipopolysaccharides; D051197:Toll-Like Receptor 4; C067980:CD68 antigen, human; D000097382:CD68 Molecule