Basic study on periodontal destruction by new T cell subset Th17

新T细胞亚群Th17破坏牙周的基础研究

• 批准号: 23593065
• 负责人: OZAKI Yukio
• 金额: $ 2.83万
• 依托单位: Nagasaki University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23593065/
• 关键词: Th17; IL-17; TLR2; TLR4; TNF-α; Th1; IL-10; 免疫組織化学; IL-23; Th 17; 骨吸収; Th2; TLR; IFN-γ; IL-4

We injected peptidoglycan (PGN) as TLR(Toll-like receptor)2 ligand and/or lipopolysaccaride (LPS) as TLR4 ligand into the gingiva in mice lower jaw. Then, the samples of gingival tissue were made with paraffin. We immunostained them with anti-tumor necrosis factor alpha (TNF-alpha) , anti-interleukin 10 (IL-10) and anti-interleukin(IL)-17. Next, We counted the TNF-alpha , IL-10 and IL-17 positive cells in them. The number of TNF-alpha and IL-10 positive cells was the most numerous in samples stimulated by the both TLR2 and 4. The samples stimulated by single TLR had less positive cells. In case of IL-17, the samples stimulated by TLR2 expressed most positive cells and the samples stimulated by TLR4 had few positive cells. Interestingly, we found the sample stimulated by both ligands also had few positive cells. These results may show that accumulation of Th17 inhibited by the other T cell subsets, for example Th1, when the mouse gingival tissues were stimulated by PGN+LPS or LPS.

我们在小鼠下颌骨的牙龈内注射了多肽聚糖(PGN)作为TLR(TLR2)配体和/或脂多糖(LPS4)作为TLR4配体。然后，用石蜡切片制取牙周组织标本。我们用抗肿瘤坏死因子α(TNF-α)、抗白介素10(IL-10)和抗白介素17(IL-17)对它们进行免疫染色。计数肿瘤坏死因子-α、白介素10、白介素17阳性细胞数。TLR2和TL4同时刺激的标本中，TNF-α和IL-10阳性细胞数最多，单独TLR刺激的标本阳性细胞数较少。在IL-17刺激下，TLR2刺激的样本表达的阳性细胞最多，而TLR4刺激的样本表达的阳性细胞较少。有趣的是，我们发现这两种配体刺激的样本中也有很少的阳性细胞。这些结果可能表明，当PGN+内毒素或内毒素刺激小鼠牙龈组织时，其他T细胞亚群如Th1抑制了Th17的聚集。