University of Pennsylvania School of Dental Medicine, Department of Microbiology, Philadelphia, PA 19104, USA.
Immunobiology. 2012 Nov;217(11):1111-6. doi: 10.1016/j.imbio.2012.07.007.
Signaling crosstalk between complement and Toll-like receptors (TLRs) normally serves to coordinate host immunity. However, the periodontal bacterium Porphyromonas gingivalis expresses C5 convertase-like enzymatic activity and adeptly exploits complement-TLR crosstalk to subvert host defenses and escape elimination. Intriguingly, this defective immune surveillance leads to the remodeling of the periodontal microbiota to a dysbiotic state that causes inflammatory periodontitis. Understanding the mechanisms by which P. gingivalis modulates complement function to cause dysbiosis offers new targets for complement therapeutics.
补体和 Toll 样受体（TLRs）之间的信号串扰通常有助于协调宿主免疫。然而，牙周细菌牙龈卟啉单胞菌表达 C5 转化酶样酶活性，并巧妙地利用补体-TLR 串扰来颠覆宿主防御并逃避清除。有趣的是，这种有缺陷的免疫监视导致牙周微生物组的重塑，导致生态失调状态，从而引起炎症性牙周炎。了解牙龈卟啉单胞菌调节补体功能导致生态失调的机制为补体治疗提供了新的靶点。
