Journal
NATURE COMMUNICATIONS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-03147-6
Keywords
-
Categories
Funding
- Japan Society for the Promotion of Science (JSPS) [15H05703, 26713015, 15H05653, 16K15252]
- Japan Agency for Medical Research and Development [JP17ek0109106]
- Kanae foundation for the promotion of medical science
- Uehara Memorial Foundation
- Kowa Life Science Foundation
- JSPS Research Fellowship for Young Scientists [15J05324]
- Grants-in-Aid for Scientific Research [16H05202, 16K15252, 15H05653, 16H05506, 17K19582, 26713015, 15J05324, 15H05703] Funding Source: KAKEN
Ask authors/readers for more resources
The immune system evolved to efficiently eradicate invading bacteria and terminate inflammation through balancing inflammatory and regulatory T-cell responses. In autoimmune arthritis, pathogenic T(H)17 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 T(H)17 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available