Hajishengallis, GeorgeLambris, John D.2023-05-222023-05-222012-11-012021-06-03https://repository.upenn.edu/handle/20.500.14332/9397Signaling 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.This manuscript version is made available under the CC-BY-NC-ND 4.0 license (http://creativecommons.org/licenses/by-nc-nd/4.0/)DentistryArticle