## C3: The Central Hub of Complement **Key Point:** C3 is the pivotal complement component that converges all three activation pathways (classical, alternative, and lectin). It is the most abundant complement protein in serum (~1.2 mg/mL) and its cleavage is essential for all downstream complement functions. ### Role of C3 in Complement Pathways ```mermaid flowchart TD A[Classical Pathway]:::outcome --> B[C4b2a convertase]:::action C[Lectin Pathway]:::outcome --> B D[Alternative Pathway]:::outcome --> E[C3bBb convertase]:::action B --> F[C3 → C3a + C3b]:::urgent E --> F F --> G[C3b amplification loop]:::action G --> H[C5 convertase formation]:::action H --> I[Terminal complement complex: C5b-9]:::outcome F --> J[Opsonization, phagocytosis, inflammation]:::action ``` ### Comparative Features of Complement Components | Component | Serum Concentration | Pathways | Function | Role | |---|---|---|---|---| | **C3** | ~1.2 mg/mL | All three | Central hub, opsonin, anaphylatoxin | Convergence point | | C1q | ~70 μg/mL | Classical only | Recognition, initiation | Early step | | C5 | ~80 μg/mL | All three | Terminal sequence | Late step | | Factor B | ~200 μg/mL | Alternative only | Convertase component | Alternative pathway | **High-Yield:** C3 cleavage generates >80% of all complement-mediated biological effects. C3b acts as an opsonin (marking pathogens for phagocytosis), and C3a is a potent anaphylatoxin. Deficiency of C3 results in severe, recurrent pyogenic infections. **Clinical Pearl:** C3 nephritic factor (C3NF) causes uncontrolled C3 activation, leading to C3 glomerulonephritis—a major cause of post-infectious glomerulonephritis and membranoproliferative GN. **Mnemonic:** "C3 = Central, Convergence, Crucial" — C3 is the central component where all three pathways meet, making it the convergence point and the most crucial for complement function.
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