Restoring Host-Microbe Homeostasis via Selective Chemoattraction of Tregs
Restoring Host-Microbe Homeostasis via Selective Chemoattraction of Tregs
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DOI：
10.1177/0022034514544300
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发表时间：
2014-09-01
影响因子：
7.6
通讯作者：
Little, S. R.
中科院分区：
文献类型：
--
作者：
Garlet, G. P.;Sfeir, C. S.;Little, S. R.
宿主-微生物在牙周病部位的稳态被破坏被认为是疾病发生和发展的关键因素。虽然负责组织损伤本身的下游机制是相对众所周知的（涉及对牙周组织破坏的各种免疫反应模式），我们才刚刚开始了解牙周环境中宿主-微生物相互作用的复杂性。不幸的是，大多数研究都集中在宿主-微生物稳态的破坏上，而不是集中在负责维持稳态的因素上。在这种情况下，调节性T细胞（TCRs）包括具有调节其它白细胞功能以避免过度免疫活化及其病理后果的独特能力的CD 4 + FOXp 3 + T细胞亚群。真菌作为宿主-微生物稳态的关键决定因素，以及病原体破坏宿主-微生物稳态后平衡宿主反应的决定因素。在牙周炎中，牙周膜起保护作用，其自然募集负责将活性病变转化为非活性病变。通过控释技术，现在可以实现TdR对牙周组织的选择性化学吸引，由于炎症免疫反应的局部控制和促修复环境的产生而减弱实验性牙周炎的演变。
The disruption of host-microbe homeostasis at the site of periodontal disease is considered a key factor for disease initiation and progress. While the downstream mechanisms responsible for the tissue damage per se are relatively well-known (involving various patterns of immune response operating toward periodontal tissue destruction), we are only beginning to understand the complexity of host-microbe interactions in the periodontal environment. Unfortunately, most of the research has been focused on the disruption of host-microbe homeostasis instead of focusing on the factors responsible for maintaining homeostasis. In this context, regulatory T-cells (Tregs) comprise a CD4+FOXp3 +T-cell subset with a unique ability to regulate other leukocyte functions to avoid excessive immune activation and its pathological consequences. Tregs act as critical determinants of host-microbe homeostasis, as well as determinants of a balanced host response after the disruption of host-microbe homeostasis by pathogens. In periodontitis, Tregs play a protective role, with their natural recruitment being responsible for conversion of active into inactive lesions. With controlled-release technology, it is now possible to achieve a selective chemoattraction of Tregs to periodontal tissues, attenuating experimental periodontitis evolution due to the local control of inflammatory immune response and the generation of a pro-reparative environment.