The complement system is a crucial part of the immune response, consisting of inactive proteins that circulate in the blood and tissues. It can be activated through three main pathways: the alternative pathway, the lectin pathway, and the classical pathway. Each pathway leads to the formation of C3 convertase, an essential enzyme in the complement cascade.
The alternative pathway is initiated when C3b, a fragment of the complement protein, binds to the surface of invading microbes. This binding triggers a series of reactions that ultimately form C3 convertase. The lectin pathway, on the other hand, is activated by mannose-binding lectin (MBL), which attaches to mannose carbohydrates on the surface of microbes. This interaction also leads to the formation of C3 convertase through a cascade of events.
The classical pathway is distinct as it involves antibodies from the adaptive immune system binding to antigens on microbes. This pathway exemplifies the synergy between innate and adaptive immunity, as the complement system enhances the immune response initiated by antibodies. Regardless of the pathway, the end result is the activation of C3 convertase, which cleaves the inactive complement protein C3 into two fragments: C3a and C3b.
C3a plays a significant role in triggering the inflammatory response, helping to eliminate pathogens, while C3b acts as an opsonin, enhancing phagocytosis by marking microbes for destruction. Additionally, C3b can interact with other complement proteins to form membrane attack complexes, which create pores in the membranes of gram-negative bacteria, leading to their lysis.
This overview of the complement system highlights its importance in both innate and adaptive immunity, illustrating how different pathways converge to enhance the body's defense mechanisms against infections.