Journal
IMMUNOLOGICAL REVIEWS
Volume 274, Issue 1, Pages 33-58Publisher
WILEY
DOI: 10.1111/imr.12500
Keywords
compstatin; convertase; immune evasion; inflammation; therapeutics
Categories
Funding
- NIH [AI068730, AI030040]
- National Science Foundation [1423304]
- European Community's Seventh Framework Programme [602699]
- Division of Computing and Communication Foundations
- Direct For Computer & Info Scie & Enginr [1423304] Funding Source: National Science Foundation
Ask authors/readers for more resources
As a preformed defense system, complement faces a delicate challenge in providing an immediate, forceful response to pathogens even at first encounter, while sparing host cells in the process. For this purpose, it engages a tightly regulated network of plasma proteins, cell surface receptors, and regulators. Complement component C3 plays a particularly versatile role in this process by keeping the cascade alert, acting as a point of convergence of activation pathways, fueling the amplification of the complement response, exerting direct effector functions, and helping to coordinate downstream immune responses. In recent years, it has become evident that nature engages the power of C3 not only to clear pathogens but also for a variety of homeostatic processes ranging from tissue regeneration and synapse pruning to clearing debris and controlling tumor cell progression. At the same time, its central position in immune surveillance makes C3 a target for microbial immune evasion and, if improperly engaged, a trigger point for various clinical conditions. In our review, we look at the versatile roles and evolutionary journey of C3, discuss new insights into the molecular basis for C3 function, provide examples of disease involvement, and summarize the emerging potential of C3 as a therapeutic target.
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