IL-10 secreting B cells regulate periodontal immune response during periodontitis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-11-07

AUTHORS

Tie Shi, Ying Jin, Yibin Miao, Ye Wang, Yong Zhou, Xiaoping Lin

ABSTRACT

Periodontitis is a disease caused by periodontopathogens and is characterized by periodontal inflammation and alveolar bone resorption. As has been proven, host immune responses incite the development and progression of periodontitis. The present study sought to establish B10 cell functions and mechanisms in regulating host immunity during periodontitis. Periodontopathogen-specific B10 cells were purified and then injected into recipients to create the adoptive transfer models. We compared inflammatory cytokines and regulatory T (Treg)/Th17 cell expression in a healthy, normal model, an experimental periodontitis model, and experimental periodontitis model adoptively transferred with B10 cells. Compared with experimental periodontitis animals, our results showed that transfer of B10 cells alleviated alveolar bone resorption (P < 0.05) by reducing periodontal osteoclastogenesis (P < 0.05). Additionally, we found that B10 cell transfer into the experimental periodontitis ones resulted in increased IL-10 (P < 0.05), but decreased IL-17 (P < 0.05) and receptor activator for nuclear factor κB ligand (RANKL) (P < 0.05) gene and protein expression in local lesions. Moreover, adoptive transfer of B10 cells reduced the proportion of Th17 cells (P < 0.05) in the gingiva. The results of our study confirmed that B10 cells can modulate local host immune responses and prevent inflammatory damage of alveolar bone by reducing pro-inflammatory cytokine expression and decreasing local proliferation of Th17 cells. More... »

PAGES

350-357

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10266-019-00470-2

DOI

http://dx.doi.org/10.1007/s10266-019-00470-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1122393872

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/31701299


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