## Type III Hypersensitivity: Immune Complex-Mediated Reactions ### Correct Statements (Options 0, 1, 3) **Key Point:** Type III hypersensitivity is **immune complex-mediated** and involves **IgG or IgM antibodies**, NOT IgE. ### Immune Complex Formation (Option 0) ```mermaid flowchart TD A[Antigen-Antibody Binding]:::action --> B{Ratio of Antigen:Antibody?}:::decision B -->|Antigen Excess| C[Small Soluble Complexes]:::outcome C --> D[Remain in Circulation<br/>Minimal Tissue Damage]:::outcome B -->|Slight Antigen Excess| E[Optimal Size Complexes]:::action E --> F[Poor Solubility<br/>Deposit in Tissues]:::outcome B -->|Antibody Excess| G[Large Lattice Complexes]:::outcome G --> H[Precipitate Locally<br/>Minimal Systemic Spread]:::outcome F --> I[Complement Activation<br/>Inflammation]:::urgent ``` **High-Yield:** The **zone of equivalence** (slight antigen excess) produces intermediate-sized complexes that are poorly soluble and deposit in vessel walls, joints, and kidneys — causing maximum tissue damage. ### Complement Activation (Option 1) | Anaphylatoxin | Effect | | --- | --- | | **C3a** | Mast cell degranulation, vasodilation, increased vascular permeability | | **C5a** | Potent neutrophil chemotaxis and activation, amplification of inflammation | | **C4a** | Minor anaphylatoxin activity | **Clinical Pearl:** C5a is the most potent anaphylatoxin and drives the neutrophilic infiltration characteristic of Type III reactions (Arthus reaction). ### Clinical Examples (Option 3) | Condition | Antigen | Antibody | Site of Deposition | | --- | --- | --- | --- | | **Serum sickness** | Foreign serum proteins (e.g., anti-venom) | IgG, IgM | Skin, joints, kidneys, blood vessels | | **Post-streptococcal GN** | Streptococcal antigen | IgG | Glomerular basement membrane | | **Systemic lupus erythematosus** | Nuclear antigens (DNA, histones) | IgG, IgM | Kidneys, skin, joints | | **Arthus reaction** | Injected antigen | IgG (local) | Skin (local vasculitis) | ### The Incorrect Statement (Option 2) **Warning:** Type III hypersensitivity is **NOT IgE-mediated**. It does NOT involve mast cells or basophils. **Mnemonic:** **Type III = IgG/IgM**, **Type I = IgE** - Type I: **I**gE, **I**mmediate (minutes) - Type III: **I**mmune complexes, **I**nflammation (hours to days) | Feature | Type I | Type III | | --- | --- | --- | | **Antibody** | IgE | IgG, IgM | | **Effector cells** | Mast cells, basophils | Neutrophils, macrophages, complement | | **Mechanism** | Degranulation → mediators | Immune complex deposition → complement → inflammation | | **Timing** | Minutes–hours | Hours–days | | **Example** | Anaphylaxis, urticaria | Serum sickness, post-streptococcal GN | **Key Point:** Type III reactions are driven by **complement activation and neutrophilic inflammation**, not by IgE-mediated mast cell degranulation.
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