Regulatory T cells attenuate experimental periodontitis progression in mice
- 10 June 2010
- journal article
- research article
- Published by Wiley in Journal of Clinical Periodontology
- Vol. 37 (7), 591-600
- https://doi.org/10.1111/j.1600-051x.2010.01586.x
Abstract
Garlet GP, Cardoso CR, Mariano FS, Claudino M, de Assis GF, Campanelli AP, Ávila‐Campos MJ, Silva JS. Regulatory T cells attenuate experimental periodontitis progression in mice. J Clin Periodontol 2010; 37: 591–600. doi: 10.1111/j.1600‐051X.2010.01586.x. Abstract Aims: The aim of this study was to identify the presence and characterize the function of regulatory T cells (Tregs) in experimental periodontitis in mice. Material and Methods: C57Bl/6 mice infected with Actinobacillus actinomycetemcomitans, treated or not with anti‐glucocorticoid‐inducible tumour necrosis factor receptor (anti‐GITR) to inhibit Tregs function, were analysed regarding inflammatory cell and Tregs influx, alveolar bone loss and cytokine expression/production (analysed by real‐time polymerase chain reaction and ELISA) throughout experimental periodontitis. Results: A. actinomycetemcomitans inoculation in mice resulted in periodontal disease characterized by marked alveolar bone loss and an influx of inflammatory cells. Flow cytometry evaluation of inflammatory cells demonstrated an increased number of CD4+CD25+ and CD4+FOXp3+ cells, characterizing the presence of Tregs in the periodontal environment in a late stage after infection. Tregs‐associated cytokines interleukin‐10 (IL‐10), cytotoxic T lymphocyte‐associated molecule 4 (CTLA‐4) and transforming growth factor‐β (TGF‐β) were found to be expressed/produced in a kinetics that resembles Tregs migration. Treatment with anti‐GITR, which inhibits Tregs function, showed increased alveolar bone loss and inflammatory cell migration. A reduction in IL‐10, CTLA‐4 and TGF‐β levels was also observed, while interferon‐γ, tumour necrosis factor‐α and receptor activator for nuclear factor κB ligand levels were increased. However, bacterial load and C‐reactive protein serum did not show any differences. Conclusion: Taken together, our results showed that the presence of Treg cells attenuates the severity of experimental periodontitis without impairment in the control of infection.Keywords
This publication has 71 references indexed in Scilit:
- B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral InfectionInterdisciplinary Perspectives on Infectious Diseases, 2009
- Experimental periodontitis in mice selected for maximal or minimal inflammatory reactions: increased inflammatory immune responsiveness drives increased alveolar bone loss without enhancing the control of periodontal infectionJournal of Periodontal Research, 2009
- Expression of receptor activator of nuclear factor‐κB ligand by B cells in response to oral bacteriaOral Microbiology and Immunology, 2009
- Diminished forkhead box P3/CD25 double-positive T regulatory cells are associated with the increased nuclear factor-kB ligand (RANKL+) T cells in bone resorption lesion of periodontal diseaseClinical and Experimental Immunology, 2007
- IFN-γ stimulates osteoclast formation and bone loss in vivo via antigen-driven T cell activationJCI Insight, 2007
- Regulatory T Cells and Human DiseaseJournal of Immunology Research, 2007
- The dual role of p55 tumour necrosis factor-α receptor inActinobacillus actinomycetemcomitans-induced experimental periodontitis: host protection and tissue destructionClinical and Experimental Immunology, 2006
- Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destructionThe Journal of Experimental Medicine, 2006
- Interleukin-10 Inhibits Gram-Negative-Microbe-Specific Human Receptor Activator of NF-κB Ligand-Positive CD4 + -Th1-Cell- Associated Alveolar Bone Loss In VivoInfection and Immunity, 2006
- IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesisJCI Insight, 1999