Three pathways, one convergence point
The complement system is a set of plasma proteins that act in a cascade. Three initiation routes feed into it: the classical pathway, triggered mainly by antibody bound to antigen; the lectin pathway, triggered by mannose-binding lectin recognizing sugar patterns on microbes; and the alternative pathway, which ticks over continuously and amplifies on surfaces lacking host regulators.
All three converge on cleavage of C3 into C3a and C3b. This central step is the hinge of the whole system, which is why C3 deficiency causes broad susceptibility to infection.
What activated complement actually does
Three effector outcomes follow convergence. Opsonization tags pathogens with C3b so phagocytes engulf them more efficiently. Small fragments such as C3a and C5a act as anaphylatoxins that recruit and activate immune cells and drive local inflammation. Finally, the terminal components assemble the membrane attack complex (MAC), a pore (C5b through C9) that can lyse certain susceptible cells.
Host cells carry regulatory proteins that restrain complement on their own surfaces, and faulty regulation is implicated in some kidney and blood disorders. This is general educational information about immunology, not medical advice.