Teng Yen-Tung A
Division of Periodontics, School of Dentistry, and Department of Microbiology & Immunology, Faculty of Medicine & Dentistry, the University of Western Ontario, London, Ontario N6A 5C1, Canada.
Crit Rev Oral Biol Med. 2003;14(4):237-52. doi: 10.1177/154411130301400402.
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.
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,我们对人类牙周疾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毒性牙周病原体方面很重要,而且在保护宿主免受牙周感染中进一步发展的破坏性状况方面也很重要。使用基因敲除和免疫缺陷小鼠品系已表明,获得性免疫反应,特别是CD4 + T细胞,在控制正在进行的感染、免疫/炎症反应以及随后宿主组织破坏方面起着关键作用。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方面的作用:(i)参与牙周发病机制的相对多样的免疫库,(ii)病原体相关的Th1-Th2细胞因子表达在牙周疾病进展中的作用,以及(iii)微生物触发的牙周CD4 + T细胞介导的破骨细胞生成因子“RANK-L”,它与原位牙槽骨破坏的诱导有关。本综述将重点关注在牙周疾病进展背景下涉及B细胞、CD8 + T细胞和CD4 + T细胞的获得性免疫反应的一些最新进展。新方法将进一步促进我们对其潜在分子机制的理解,这可能会导致开发针对牙周疾病及其相关并发症的新治疗方式。