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J Dent Res. 2014 Sep;93(9):834-9. doi: 10.1177/0022034514544300. Epub 2014 Jul 23.

Restoring host-microbe homeostasis via selective chemoattraction of Tregs.

Author information

1
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University (FOB/USP), Bauru, SP, Brazil garletgp@usp.br.
2
Bioengineering The McGowan Institute for Regenerative Medicine Department of Oral Biology The Center for Craniofacial Regeneration, University of Pittsburgh, Pittsburgh, PA, USA.
3
Departments of Chemical Engineering Bioengineering Immunology The McGowan Institute for Regenerative Medicine The Center for Craniofacial Regeneration, University of Pittsburgh, Pittsburgh, PA, USA.

Abstract

The disruption of host-microbe homeostasis at the site of periodontal disease is considered a key factor for disease initiation and progress. While the downstream mechanisms responsible for the tissue damage per se are relatively well-known (involving various patterns of immune response operating toward periodontal tissue destruction), we are only beginning to understand the complexity of host-microbe interactions in the periodontal environment. Unfortunately, most of the research has been focused on the disruption of host-microbe homeostasis instead of focusing on the factors responsible for maintaining homeostasis. In this context, regulatory T-cells (Tregs) comprise a CD4+FOXp3 +T-cell subset with a unique ability to regulate other leukocyte functions to avoid excessive immune activation and its pathological consequences. Tregs act as critical determinants of host-microbe homeostasis, as well as determinants of a balanced host response after the disruption of host-microbe homeostasis by pathogens. In periodontitis, Tregs play a protective role, with their natural recruitment being responsible for conversion of active into inactive lesions. With controlled-release technology, it is now possible to achieve a selective chemoattraction of Tregs to periodontal tissues, attenuating experimental periodontitis evolution due to the local control of inflammatory immune response and the generation of a pro-reparative environment.

KEYWORDS:

bone regeneration; chemokines; drug delivery systems; inflammation; periodontal disease(s)/periodontitis; regulatory T-Lymphocytes

PMID:
25056995
PMCID:
PMC4213252
DOI:
10.1177/0022034514544300
[Indexed for MEDLINE]
Free PMC Article

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