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破骨细胞样 T 细胞对口腔微生物群的防御作用。

Host defense against oral microbiota by bone-damaging T cells.

机构信息

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, 113-0033, Tokyo, Japan.

Department of Molecular Biology and Biochemistry, Biomedical Sciences Major, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3, Kasumi, Minami-ku, Hiroshima, 734-8553, Japan.

出版信息

Nat Commun. 2018 Feb 16;9(1):701. doi: 10.1038/s41467-018-03147-6.

Abstract

The immune system evolved to efficiently eradicate invading bacteria and terminate inflammation through balancing inflammatory and regulatory T-cell responses. In autoimmune arthritis, pathogenic T17 cells induce bone destruction and autoimmune inflammation. However, whether a beneficial function of T-cell-induced bone damage exists is unclear. Here, we show that bone-damaging T cells have a critical function in the eradication of bacteria in a mouse model of periodontitis, which is the most common infectious disease. Bacterial invasion leads to the generation of specialized T17 cells that protect against bacteria by evoking mucosal immune responses as well as inducing bone damage, the latter of which also inhibits infection by removing the tooth. Thus, bone-damaging T cells, which may have developed to stop local infection by inducing tooth loss, function as a double-edged sword by protecting against pathogens while also inducing skeletal tissue degradation.

摘要

免疫系统的进化旨在通过平衡炎症和调节性 T 细胞反应,有效地清除入侵的细菌并终止炎症。在自身免疫性关节炎中,致病性 T17 细胞会诱导骨破坏和自身免疫炎症。然而,T 细胞诱导的骨损伤是否具有有益功能尚不清楚。在这里,我们发现在牙周炎的小鼠模型中,破坏骨的 T 细胞在清除细菌方面具有关键作用,牙周炎是最常见的传染病。细菌入侵会导致产生专门的 T17 细胞,通过引发黏膜免疫反应以及诱导骨损伤来保护免受细菌侵害,后者也通过去除牙齿来抑制感染,从而发挥作用。因此,破坏骨的 T 细胞可能是为了通过诱导牙齿脱落来阻止局部感染而发展起来的,它们既可以作为保护病原体的双刃剑,也可以诱导骨骼组织降解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54c9/5816021/65d6f9841f41/41467_2018_3147_Fig1_HTML.jpg

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