title: T-lymphocyte and cytokine expression in human inflammatory periapical lesions.
abstract: BACKGROUND
  Lymphocytes, among many cells, express different sets of cytokines, chemokines, and receptors, which are considered important mediators of periapical immune response to infection.
  
  
  METHODS
  The aim of this study was to evaluate the mRNA expression of CD4(+)CD28(+) and CD8(+) T genes and the gene expression of interferon-γ, tumor necrosis factor-α, interleukin (IL)-1β, IL-17A, IL-10, CCL2/MCP-1, CCL4, CCL5, CXCR4, CCR5, and receptor activator for nuclear factor kappa B ligand (RANKL) in periapical interstitial fluid from human root canal infections. The samples were collected immediately after root canal cleaning and 7 days later (restrained root canal bacterial load) to characterize those gene expressions.
  
  
  RESULTS
  Real-time polymerase chain reaction demonstrated significantly higher levels of CD4(+)CD28(+) and CD8(+) T-cell markers in the former root canal condition and an increase of IL-10 and CXCR4, followed by a decrease of proinflammatory cytokines such as RANKL, interferon-γ, IL-1β, and CCL5.
  
  
  CONCLUSIONS
  Analyses of T-lymphocyte and cytokine expression in periapical area were able to show that distinct root canal conditions might play regulatory roles in controlling local immune/inflammatory processes.
authors.affiliation: Departamento de Odontologia Restauradora, Faculdade de Odontologia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: Luciana Carla Neves
authors.initials: LC
authors.lastname: de Brito
authors.forename: Flávia Rocha Fonseca
authors.initials: FR
authors.lastname: Teles
authors.forename: Ricardo Palmier
authors.initials: RP
authors.lastname: Teles
authors.forename: Antônio Helvécio
authors.initials: AH
authors.lastname: Totola
authors.forename: Leda Quércia
authors.initials: LQ
authors.lastname: Vieira
authors.forename: Antônio Paulino Ribeiro
authors.initials: AP
authors.lastname: Sobrinho
mesh_terms: D001424:Bacterial Infections / Q000276:immunology; D018106:CD28 Antigens / Q000032:analysis; D015704:CD4 Antigens / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016827:CD8 Antigens / Q000032:analysis; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D018932:Chemokine CCL2 / Q000032:analysis; D054407:Chemokine CCL4 / Q000032:analysis; D018946:Chemokine CCL5 / Q000032:analysis; D016207:Cytokines / Q000032:analysis*; D003790:Dental Pulp Necrosis / Q000276:immunology / Q000382:microbiology; D045604:Extracellular Fluid / Q000276:immunology; D005500:Follow-Up Studies; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D007371:Interferon-gamma / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D020381:Interleukin-17 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D010485:Periapical Periodontitis / Q000276:immunology*; D053245:RANK Ligand / Q000032:analysis; D019713:Receptors, CCR5; D019718:Receptors, CXCR4; D012390:Root Canal Therapy; D013601:T-Lymphocytes / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: C111835:CCL2 protein, human; C483024:CCL5 protein, human; D018106:CD28 Antigens; D015704:CD4 Antigens; D016827:CD8 Antigens; C527276:CXCR4 protein, human; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D016207:Cytokines; C508609:IL10 protein, human; C508717:IL17A protein, human; D018836:Inflammation Mediators; D020381:Interleukin-17; D053583:Interleukin-1beta; D053245:RANK Ligand; D019713:Receptors, CCR5; D019718:Receptors, CXCR4; C505688:TNFSF11 protein, human; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma