title: Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease.
abstract: BACKGROUND
  Periodontal disease is a chronic inflammation of the attachment structures of the teeth, triggered by potentially hazardous microorganisms and the consequent immune-inflammatory responses. In humans, the T helper type 17 (Th17) lineage, characterized by interleukin-17 (IL-17) production, develops under transforming growth factor-beta (TGF-beta), IL-1beta, and IL-6 signaling, while its pool is maintained by IL-23. Although this subset of cells has been implicated in various autoimmune, inflammatory, and bone-destructive conditions, the exact role of T lymphocytes in chronic periodontitis is still controversial. Therefore, in this study we investigated the presence of Th17 cells in human periodontal disease.
  
  
  METHODS
  Gingival and alveolar bone samples from healthy patients and patients with chronic periodontitis were collected and used for the subsequent assays. The messenger RNA expression for the cytokines IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 in gingiva or IL-17 and receptor activator for nuclear factor-kappaB ligand in alveolar bone was evaluated by real-time polymerase chain reaction. The production of IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 proteins was evaluated by immunohistochemistry and the presence of Th17 cells in the inflamed gingiva was confirmed by immunofluorescence confocal microscopy for CD4 and IL-17 colocalization.
  
  
  RESULTS
  Our data demonstrated elevated levels of IL-17, TGF-beta, IL-1beta, IL-6, and IL-23 messenger RNA and protein in diseased tissues as well as the presence of Th17 cells in gingiva from patients with periodontitis. Moreover, IL-17 and the bone resorption factor RANKL were abundantly expressed in the alveolar bone of diseased patients, in contrast to low detection in controls.
  
  
  CONCLUSIONS
  These results provided strong evidence for the presence of Th17 cells in the sites of chronic inflammation in human periodontal disease.
authors.affiliation: Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
authors.forename: C R
authors.initials: CR
authors.lastname: Cardoso
authors.forename: G P
authors.initials: GP
authors.lastname: Garlet
authors.forename: G E
authors.initials: GE
authors.lastname: Crippa
authors.forename: A L
authors.initials: AL
authors.lastname: Rosa
authors.forename: W M
authors.initials: WM
authors.lastname: Júnior
authors.forename: M A
authors.initials: MA
authors.lastname: Rossi
authors.forename: J S
authors.initials: JS
authors.lastname: Silva
mesh_terms: D000328:Adult; D016301:Alveolar Bone Loss / Q000276:immunology* / Q000378:metabolism; D016022:Case-Control Studies; D055113:Chronic Periodontitis / Q000276:immunology*; D005260:Female; D005455:Fluorescent Antibody Technique; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D020381:Interleukin-17 / Q000096:biosynthesis*; D053583:Interleukin-1beta / Q000096:biosynthesis; D053759:Interleukin-23 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D018613:Microscopy, Confocal; D053245:RANK Ligand / Q000096:biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000096:biosynthesis
chemical_list: D020381:Interleukin-17; D053583:Interleukin-1beta; D053759:Interleukin-23; D015850:Interleukin-6; D053245:RANK Ligand; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta