获得性免疫与牙周病进展的关系。

Yen-Tung A Teng
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引用次数: 167

摘要

由于缺乏特异性和敏感性的工具或模型来研究复杂的微生物挑战及其与宿主免疫系统的相互作用,我们对人类牙周病发病机制的理解受到限制。细胞和分子生物学研究的最新进展表明,获得性免疫系统不仅在对抗恶性牙周病原体方面具有重要作用,而且在保护宿主免受牙周感染的进一步破坏方面也具有重要作用。基因敲除和免疫缺陷小鼠菌株的使用表明,获得性免疫反应,特别是CD4+ t细胞,在控制持续感染、免疫/炎症反应和随后的宿主组织破坏中起着关键作用。特别是,对病原体特异性CD4+ t细胞介导的免疫的研究已经阐明了以下因素的作用:(i)参与牙周发病的相对多样化的免疫库,(ii)病原体相关的Th1-Th2细胞因子表达在牙周病进展中的作用,以及(iii)微生物触发的牙周CD4+ t细胞介导的破骨因子“RANK-L”,它与诱导牙槽骨原位破坏有关。本文将对近期在牙周病进展中涉及b细胞、CD8+ t细胞和CD4+ t细胞的获得性免疫反应的研究进展进行综述。新的方法将进一步促进我们对其潜在分子机制的理解,这可能导致牙周病及其相关并发症的新治疗方式的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of acquired immunity and periodontal disease progression.

Our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system not only in fighting the virulent periodontal pathogens but also in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response-in particular, CD4+ T-cells-plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction. In particular, studies of the pathogen-specific CD4+ T-cell-mediated immunity have clarified the roles of: (i) the relative diverse immune repertoire involved in periodontal pathogenesis, (ii) the contribution of pathogen-associated Th1-Th2 cytokine expressions in periodontal disease progression, and (iii) micro-organism-triggered periodontal CD4+ T-cell-mediated osteoclastogenic factor, 'RANK-L', which is linked to the induction of alveolar bone destruction in situ. The present review will focus on some recent advances in the acquired immune responses involving B-cells, CD8+ T-cells, and CD4+ T-cells in the context of periodontal disease progression. New approaches will further facilitate our understanding of their underlying molecular mechanisms that may lead to the development of new treatment modalities for periodontal diseases and their associated complications.

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