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Complement and Host Defence Against Microorganisms

INTRODUCTION The complement system is a series of sequentially activated extracellular proteins, which occupy an important role in the humoral defence system against microorganisms. Activation of the complement system occurs in a precise sequence of biochemical steps, often occurring by proteolytic cleavage of the complement protein into a large fragment (termed, with the exception of C2, “b”, e.g. C3b) and a small fragment (termed “a”, e.g. C3a). The large fragment remains attached to the activating surface and complement activation continues, while smaller fragments are released into the fluid-phase where they have a wide range of biological effects on host cells, enhancing host defence mechanisms and inflammation. A number of cell-associated and circulating regulatory proteins, which do not require activation, modulate complement activity and prevent uncontrolled complement deposition. Activation of the complement system results in covalent deposition of the important opsonic protein, C3b, onto the surface of microorganisms. Interaction of bound complement fragments with specific receptors on phagocytic cells promotes phagocytosis. Alternatively, the “membrane-attack complex”, CSb-9, may be assembled with the resultant lysis of susceptible Gram-negative bacteria. This review will focus on the biochemical mechanism of C3b attachment to foreign surfaces, especially microorganisms, and on details of the subsequent interaction between complement-coated bacteria and specific receptors for C3 fragments on phagocytic cells. A glossary of complement terminology is shown in Table 1.