Opsonins, like C3b, play a crucial role in enhancing the phagocytosis of pathogens by binding to their surfaces. This enhances recognition by phagocytic cells and facilitates engulfment, ultimately increasing the efficiency of the phagocytic process. Complement receptors CR1, CR2, and CR3 also play specific roles in recognizing and clearing opsonized pathogens.

Complement C3 protein generates C3a and C3b, crucial in immune response. C3a induces inflammation by binding to immune cells, aiding pathogen combat. C3b enhances pathogen recognition, improving phagocytosis. Bound to pathogens, C3b initiates the membrane attack complex, creating pores for pathogen lysis. Together, they efficiently eliminate pathogens and maintain immune balance.

The complement system has three initiation pathways: classical, lectin, and alternative. Each has distinct triggers but converges at C3 convertase formation, crucial for the complement cascade. The pathways differ in initiation triggers and key components, but all activate C3, which marks pathogens for destruction. C3 convertase amplifies the cascade, leading to pathogen elimination.