Page 118 - Veterinary Immunology, 10th Edition

VetBooks.ir Other Consequences of Complement

Activation

Although microbial destruction mediated by terminal complement
complexes is the most obvious beneficial activity of the complement
system, its protective effects go far beyond this.

Opsonization

Bacteria normally lack complement regulators so that uncontrolled
complement activation occurs on their surface. This leads to
proinflammatory signaling, opsonization, phagocytosis, and in
some organisms, especially Gram-negative bacteria and some

parasites, TCC assembly and bacterial lysis. C3b and C4b are very
effective opsonins (Chapter 5). Phagocytic cells express CR1, and
tissue macrophages also express CRIg. C3b-coated organisms will

be bound to these cells and undergo type II phagocytosis (Chapter
5). If for some reason these organisms cannot be ingested,
neutrophils may secrete their lysosomal enzymes and oxidants into
the surrounding tissue fluid. This can cause inflammation and
tissue damage, a reaction classified as type III hypersensitivity

(Chapter 32). Given the long evolutionary history of the
complement system, it is not surprising that many bacteria have
evolved mechanisms to neutralize the effects of complement

(Chapter 26)

Removal of Apoptotic Cells

Complement contributes to recovery from inflammation by
promoting the removal of apoptotic cells and immune complexes.

Apoptotic cells lose their complement inhibitors CD46 and CD59.
As a result, they are opsonized by C3b and C4b and removed by
phagocytosis. Apoptotic cells also bind CRP that can then bind C1q,
leading to classical pathway activation. Properdin (FP) binds to

apoptotic T cells, resulting in C3b-mediated opsonization and
destruction.

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