Journal
MOLECULAR ORAL MICROBIOLOGY
Volume 31, Issue 1, Pages 3-17Publisher
WILEY
DOI: 10.1111/omi.12129
Keywords
C3; complement; compstatin Cp40; inflammation, periodontitis; primate models; therapeutics
Categories
Funding
- US National Institutes of Health [DE015254, DE017138, DE021685, DE024716, AI003040, AI068730, EY020633, GM097747]
- European Community's Seventh Framework Program [602699]
- Greek General Secretariat for Research and Technology
- European Regional Development Fund under the Action 'Development Grants For Research Institutions - KRIPIS' of OPCE II
Ask authors/readers for more resources
There is increasing appreciation that complement dysregulation lies at the heart of numerous immune-mediated and inflammatory disorders. Complement inhibitors are therefore being evaluated as new therapeutic options in various clinical translation programs and the first clinically approved complement-targeted drugs have profoundly impacted the management of certain complement-mediated diseases. Among the many members of the intricate protein network of complement, the central component C3 represents a 'hot-spot' for complement-targeted therapeutic intervention. C3 modulates both innate and adaptive immune responses and is linked to diverse immunomodulatory systems and biological processes that affect human pathophysiology. Compelling evidence from preclinical disease models has shown that C3 interception may offer multiple benefits over existing therapies or even reveal novel therapeutic avenues in disorders that are not commonly regarded as complement-driven, such as periodontal disease. Using the clinically developed compstatin family of C3 inhibitors and periodontitis as illustrative examples, this review highlights emerging therapeutic concepts and developments in the design of C3-targeted drug candidates as novel immunotherapeutics for oral and systemic inflammatory diseases.
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