Host defense against oral microbiota by bone-damaging T cells.
Masayuki TsukasakiNoriko KomatsuKazuki NagashimaTakeshi NittaWarunee PluemsakunthaiChisa ShukunamiYoichiro IwakuraTomoki NakashimaKazuo OkamotoHiroshi TakayanagiPublished in: Nature communications (2018)
The immune system evolved to efficiently eradicate invading bacteria and terminate inflammation through balancing inflammatory and regulatory T-cell responses. In autoimmune arthritis, pathogenic TH17 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 TH17 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.
Keyphrases
- bone mineral density
- oxidative stress
- soft tissue
- induced apoptosis
- bone regeneration
- bone loss
- mouse model
- immune response
- multiple sclerosis
- palliative care
- postmenopausal women
- cell cycle arrest
- rheumatoid arthritis
- inflammatory response
- body composition
- drug induced
- cell migration
- cell death
- helicobacter pylori infection
- multidrug resistant
- endothelial cells