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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.
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Hajishengallis, G., & Lambris, J. D. (2012). Complement and Dysbiosis in Periodontal Disease. Immunobiology, 217 (11), 1111-1116. http://dx.doi.org/10.1016/j.imbio.2012.07.007
Date Posted: 24 February 2022
This document has been peer reviewed.