Regulatory T-cells in periapical lesions

J Dent Res. 2009 Nov;88(11):997-1002. doi: 10.1177/0022034509347090.

Abstract

CD4(+)CD25(hi)Foxp3(+) regulatory T-cells (Tregs) are of crucial importance in regulating the immune response, including the control of any defense against infection. Their presence in periapical lesions has not been demonstrated, as yet. We hypothesized that Tregs infiltrate periapical lesions, where they inhibit T-cell proliferation. The aim of this study was to characterize Tregs in periapical lesions by confocal microscopy, flow cytometry, and functional assays. We showed that CD4(+)CD25(hi)Foxp3(+) cells in periapical lesions expressed IL-10 and TGF-beta. Their frequency was significantly higher than in peripheral blood and correlated with the levels of TGF-beta and IL-10 in culture supernatants of periapical lesion mononuclear cells. Tregs inhibited the proliferation of responder T-cells in vitro, at least in part, by stimulating the production of IL-10. These findings suggest that CD4(+)CD25(hi)Foxp3(+) cells in periapical lesions may play regulatory roles in controlling local immune/inflammatory processes.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • CD4 Antigens / immunology
  • CD4 Lymphocyte Count
  • Cell Proliferation
  • Cells, Cultured
  • Coculture Techniques
  • Flow Cytometry
  • Forkhead Transcription Factors / immunology
  • Glucocorticoid-Induced TNFR-Related Protein
  • Humans
  • Interleukin-10 / immunology
  • Interleukin-2 Receptor alpha Subunit / immunology
  • Leukocytes, Mononuclear / immunology
  • Lymphocyte Activation / immunology
  • Microscopy, Confocal
  • Middle Aged
  • Periapical Diseases / immunology*
  • Receptors, Nerve Growth Factor / immunology
  • Receptors, Tumor Necrosis Factor / immunology
  • T-Lymphocytes, Regulatory / immunology*
  • Transforming Growth Factor beta / immunology
  • Young Adult

Substances

  • CD4 Antigens
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Glucocorticoid-Induced TNFR-Related Protein
  • IL2RA protein, human
  • Interleukin-2 Receptor alpha Subunit
  • Receptors, Nerve Growth Factor
  • Receptors, Tumor Necrosis Factor
  • TNFRSF18 protein, human
  • Transforming Growth Factor beta
  • Interleukin-10