## Membrane Attack Complex (MAC) Formation ### Sequential Assembly of MAC The membrane attack complex is the terminal effector of complement, formed by sequential binding of C5b through C9: ```mermaid flowchart LR A[C5 cleavage] -->|C5a + C5b| B[C5b binds membrane]:::action B --> C[C6 + C7 bind]:::action C --> D[C5b-6-7 complex]:::outcome D --> E[C8 inserts into bilayer]:::action E --> F[Small pore formed]:::outcome F --> G[C9 polymerizes]:::action G --> H[Complete MAC pore]:::outcome H --> I[Cell lysis]:::urgent ``` ### Components of MAC | Component | Role | Function | | --- | --- | --- | | **C5b** | Nucleation site | Anchors complex to membrane; initiates assembly | | **C6** | Binding partner | Stabilizes C5b; prevents inactivation | | **C7** | Binding partner | Increases hydrophobicity; inserts into bilayer | | **C8** | Pore initiator | Creates small pore (10 Å); allows ion leakage | | **C9** | Pore enlarger | Polymerizes (10–16 molecules); enlarges pore to 100 Å | **Key Point:** C9 (not C2) is the final component that polymerizes to form the complete, large pore. C2 is a component of the **classical and lectin pathway C3 convertase** (C4b2a), NOT the MAC. ### Why This Patient Has Recurrent Meningitis **High-Yield:** Deficiencies in **terminal complement components (C5–C9)** or **alternative pathway components (Factor H, Factor I, Properdin)** specifically increase susceptibility to **Neisseria meningitidis** and **Neisseria gonorrhoeae**. This patient's normal C3/C4 but absent bactericidal activity suggests a terminal pathway defect (likely C5–C9 or C3b deposition defect). **Clinical Pearl:** Patients with recurrent meningococcal infections should receive meningococcal vaccination and prophylactic antibiotics. Complement deficiency screening includes hemolytic assay (CH50 for classical, AP50 for alternative).
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.