Type VI Hypersensitivity Reaction (Antibody-mediated cellular dysfunction)
Type VI hypersensitivity is a rarely described variant in some classifications, referring to antibody-mediated dysfunction of cellular activity, not causing direct cytotoxicity or inflammation.
- Sometimes used interchangeably with Type V, but some sources distinguish Type VI as focusing specifically on inhibitory (blocking) effects, while Type V includes both stimulating and blocking.
Key Features
- Mediated by: IgG autoantibodies.
- No cell lysis or complement-mediated destruction.
- Antibodies alter cellular functions, especially by blocking receptor-mediated signaling.
- Leads to loss of function, rather than tissue destruction.
Mechanism
- Autoantibodies bind to cell surface receptors or associated proteins.
- They inhibit receptor-ligand interactions, preventing normal signaling and function.
- Do not induce complement activation or ADCC.
Clinical Example
Difference from Type V
Pathogenesis Example: Myasthenia Gravis
- IgG autoantibodies target acetylcholine receptors.
- Block acetylcholine binding at neuromuscular junction.
- Decreased end-plate potential → impaired muscle contraction.
- Results in muscle weakness and fatigue.
Diagnostic Tests
- Detection of specific autoantibodies in serum.
- Anti-acetylcholine receptor antibodies (myasthenia gravis).
- Anti-intrinsic factor antibodies (pernicious anemia).
Treatment
- Immunosuppression (e.g., corticosteroids, azathioprine).
- Plasmapheresis (to remove antibodies in severe cases).
- Disease-specific supportive therapy (e.g., cholinesterase inhibitors for myasthenia gravis).