Page 119 - Veterinary Immunology, 10th Edition

Inflammation
VetBooks.ir Complement activation results in inflammation and possibly tissue

damage. The anaphylatoxin C5a enhances TLR-induced production

of TNF-α, IL-1β, and IL-6. After binding to its receptor, it also
interacts with toll-like receptor 2 (TLR2), TLR4, and TLR9. This TLR
stimulation enhances cellular expression of C3aR and C5aR.

Blood Coagulation

The complement system enhances blood coagulation and inhibits
fibrinolysis. Thus C5a induces the expression of tissue factor and
plasminogen activator inhibitor I. Likewise, components of the

clotting system amplify the complement system. Activated clotting
factor XII can cleave C1, and so activate the classical pathway.
Thrombin acts on C5 to generate C5a.

Chemotaxis

Activation of the complement system generates chemotactic
peptides, including C5a and C5b67 (Table 4.2). C5b67 attracts
neutrophils and eosinophils, whereas C5a attracts not only

neutrophils and eosinophils but also macrophages and basophils.
C5a also stimulates the neutrophil respiratory burst and
upregulates CR1 and integrin expression.

TABLE 4.2

Complement-Derived Chemotactic Factors

Factor Target
C3a Eosinophils
C5a Neutrophils, eosinophils, macrophages
C567 Neutrophils, eosinophils
FBb Neutrophils
C3e Promotes leukocytosis

Immune Regulation

The complement system regulates both humoral and cell-mediated

adaptive immunity. Thus C3d binds to antigen. When an antigen
molecule binds to a B cell antigen receptor, any attached C3d will

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