Singhatanadgit Weerachai, Kitpakornsanti Setthawut, Toso Montree, Pavasant Prasit
Oral and Maxillofacial Surgery Unit, Faculty of Dentistry, Thammasat University, Rangsit Campus, Pathumthani, Thailand.
Research Unit in Mineralized Tissue Reconstruction, Thammasat University, Rangsit Campus, Pathumthani, Thailand.
R Soc Open Sci. 2022 Jul 27;9(7):220056. doi: 10.1098/rsos.220056. eCollection 2022 Jul.
Periodontal ligament (PDL) cells help maintain tissue homeostasis by balancing PDL tissue inflammation and regeneration. However, the mechanisms by which interferon γ (IFNγ) modulate this process are not yet fully understood. The present study aimed to examine the effect of primed and non-primed PDL cells with IFNγ on the viability and differentiation of T lymphocytes and its functional consequences. The results showed that IFNγ-primed PDL cells possessed enhanced immunosuppression by suppressing T-lymphocyte viability and directing T-lymphocyte differentiation towards a higher T helper (Th) Th2/Th1 ratio. Suppression of T-cell viability was mainly mediated by IFNγ-inducible secreted mediators, which was prevented in the presence of direct cell contact, probably by intercellular adhesion molecule-1 (ICAM-1)-induced PI3 K-mediated transforming growth factor β1 expression in PDL cells. By contrast, ICAM-1 activation augmented IFNγ-induced IFNγ and interleukin-6 expression in PDL cells, which in turn modulated T-cell differentiation. The resulting interaction between these two cell types activated macrophage and suppressed osteoclast differentiation. In conclusion, the results have shown, for the first time to our knowledge, that primed and non-primed PDL cells with IFNγ differentially control T-cell responses via IFNγ-inducible mediators and ICAM-1-mediated direct cell contact, suggesting the role of PDL cells in shifting an inflammatory phase towards a regenerative phase.
牙周膜（PDL）细胞通过平衡牙周膜组织的炎症和再生来帮助维持组织稳态。然而，干扰素γ（IFNγ）调节这一过程的机制尚未完全明确。本研究旨在探讨经IFNγ预处理和未经预处理的PDL细胞对T淋巴细胞活力和分化的影响及其功能后果。结果显示，经IFNγ预处理的PDL细胞通过抑制T淋巴细胞活力并使T淋巴细胞分化倾向于更高的辅助性T细胞（Th）Th2/Th1比值，从而增强免疫抑制作用。T细胞活力的抑制主要由IFNγ诱导的分泌介质介导，而在存在直接细胞接触时这种抑制作用被阻止，这可能是通过细胞间黏附分子-1（ICAM-1）诱导的PI3 K介导的PDL细胞中转化生长因子β1表达实现的。相比之下，ICAM-1激活增强了IFNγ诱导的PDL细胞中IFNγ和白细胞介素-6的表达，进而调节T细胞分化。这两种细胞类型之间的相互作用激活了巨噬细胞并抑制了破骨细胞分化。总之，据我们所知，结果首次表明，经IFNγ预处理和未经预处理的PDL细胞通过IFNγ诱导的介质和ICAM-1介导的直接细胞接触以不同方式控制T细胞反应，提示PDL细胞在将炎症阶段转变为再生阶段中的作用。
