Review of the Complement System: Videos & Practice Problems

The complement system can be activated through three distinct pathways: the alternative pathway, the lectin pathway, and the classical pathway. The alternative pathway is triggered by the binding of C3b to the surface of invading microbes. The lectin pathway is activated when mannose-binding lectin (MBL) binds to mannose carbohydrates on the surface of microbes. The classical pathway is initiated when antibodies from the adaptive immune system bind to antigens on the surface of microbes. All three pathways converge at the formation of C3 convertase, which cleaves the inactive protein C3 into C3a and C3b, leading to various immune responses.

The classical pathway of the complement system is activated when antibodies from the adaptive immune system bind to antigens on the surface of microbes. This binding triggers a cascade of events that ultimately leads to the formation of C3 convertase. C3 convertase then cleaves the inactive complement protein C3 into C3a and C3b. C3a triggers inflammation, while C3b acts as an opsonin to enhance phagocytosis and can also lead to the formation of membrane attack complexes that lyse microbial cells. This pathway highlights the interplay between innate and adaptive immunity, as it involves antibodies from the adaptive immune system to activate the complement system, which is part of innate immunity.

C3 convertase is a crucial enzyme in the complement system that is formed through the activation of any of the three pathways: alternative, lectin, or classical. Its primary role is to cleave the inactive complement protein C3 into two fragments: C3a and C3b. C3a is involved in triggering the inflammatory response, which helps to eliminate microbes. C3b acts as an opsonin, enhancing the effectiveness of phagocytosis by making it easier for phagocytes like macrophages to engulf microbes. Additionally, C3b can interact with other complement proteins to form membrane attack complexes that create pores in microbial cell membranes, leading to cell lysis.

In the complement system, C3a and C3b have distinct but complementary roles. C3a primarily functions to trigger the inflammatory response, which helps to recruit immune cells to the site of infection and eliminate microbes. On the other hand, C3b acts as an opsonin, which means it tags microbes for easier recognition and ingestion by phagocytes like macrophages. Additionally, C3b can interact with other complement proteins to form membrane attack complexes that create pores in the membranes of microbial cells, leading to their lysis. Together, C3a and C3b play crucial roles in enhancing the immune response against pathogens.

The complement system serves as a bridge between innate and adaptive immunity. It is part of the innate immune system but can be activated by components of the adaptive immune system, such as antibodies. This interaction is most evident in the classical pathway, where antibodies from the adaptive immune system bind to antigens on the surface of microbes, triggering the complement cascade. This crosstalk enhances the overall immune response, as the complement system can amplify the effects of antibodies, leading to more effective pathogen elimination through processes like opsonization, inflammation, and cell lysis.