Regulatory T cell phenotype and anti-osteoclastogenic function in experimental periodontitis.
Regulatory T cell phenotype and anti-osteoclastogenic function in experimental periodontitis.
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实验性牙周炎中调节性T细胞表型和抗破骨细胞生成功能的研究
DOI:
10.1038/s41598-020-76038-w
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发表时间:
2020-11-04
影响因子:
4.6
通讯作者:
Kantarci A
中科院分区:
文献类型:
--
作者:
Alvarez C;Suliman S;Almarhoumi R;Vega ME;Rojas C;Monasterio G;Galindo M;Vernal R;Kantarci A
The alveolar bone resorption is a distinctive feature of periodontitis progression and determinant for tooth loss. Regulatory T lymphocytes (Tregs) display immuno-suppressive mechanisms and tissue repairing functions, which are critical to support periodontal health. Tregs may become unstable and dysfunctional under inflammatory conditions, which can even accelerate tissue destruction. In this study, experimental periodontitis was associated with the progressive and increased presence of Th17 and Treg-related mediators in the gingiva (IL-6, IL-17A, IL-17F, RANKL, IL-10, TGF-β and GITR; P < 0.05), and the proliferation of both Treg and Th17 cells in cervical lymph nodes. Tregs from cervical lymph nodes had reduced Foxp3 expression (> 25% MFI loss) and increased IL-17A expression (> 15%), compared with Tregs from spleen and healthy controls. Tregs gene expression analysis showed a differential signature between health and disease, with increased expression of Th17-associated factors in periodontitis-derived Tregs. The ex vivo suppression capacity of Tregs on osteoclastic differentiation was significantly lower in Tregs obtained from periodontally diseased animals compared to controls (P < 0.05), as identified by the increased number of TRAP+ osteoclasts (P < 0.01) in the Tregs/pre-osteoclast co-cultures. Taken together, these results demonstrate that Tregs become phenotypically unstable and lose anti-osteoclastogenic properties during experimental periodontitis; thus, further promoting the Th17-driven bone loss.
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影响因子:
4.6
作者:
Alvarez C;Rojas C;Rojas L;Cafferata EA;Monasterio G;Vernal R
通讯作者:
Vernal R
影响因子:
6.4
作者:
Lin, Danping;Li, Lu;Xu, Yan
通讯作者:
Xu, Yan
影响因子:
18.6
作者:
Hajishengallis G;Korostoff JM
通讯作者:
Korostoff JM
影响因子:
2.2
作者:
Abe, Toshiharu;Hajishengallis, George
通讯作者:
Hajishengallis, George
影响因子:
17.1
作者:
Dutzan N;Kajikawa T;Abusleme L;Greenwell-Wild T;Zuazo CE;Ikeuchi T;Brenchley L;Abe T;Hurabielle C;Martin D;Morell RJ;Freeman AF;Lazarevic V;Trinchieri G;Diaz PI;Holland SM;Belkaid Y;Hajishengallis G;Moutsopoulos NM
通讯作者:
Moutsopoulos NM