Type V Hypersensitivity Reaction (Antibody-mediated cellular stimulation/inhibition)
Type V hypersensitivity is an antibody-mediated reaction in which antibodies bind to cell surface receptors, stimulating or inhibiting their function without causing cell destruction.
- It is sometimes considered a variant of type II hypersensitivity, but with functional rather than cytotoxic effects.
- Also known as receptor-mediated hypersensitivity.
Key Features
- Mediated by: IgG (mostly).
- Antibodies act as agonists (stimulate receptor) or antagonists (block receptor).
- No complement-mediated cytotoxicity or direct cell lysis.
Mechanisms
- 1 Stimulatory effect (agonistic)
- Antibody binds to receptor → mimics natural ligand → causes continuous stimulation.
- 2 Inhibitory effect (antagonistic)
- Antibody binds to receptor → blocks normal ligand binding → inhibits normal cell signaling.
Clinical Examples
Differences from Type II
Pathogenesis in Graves’ disease (example)
- Autoantibodies develop against TSH receptor.
- Antibody acts as a TSH agonist → stimulates thyroid hormone synthesis and secretion.
- Results in thyrotoxicosis (hyperthyroidism).
Diagnostic Tests
- Serological tests for specific autoantibodies, e.g.:
- TSH receptor antibodies in Graves’ disease.
- Acetylcholine receptor antibodies in myasthenia gravis.
Treatment
- Immunosuppressive therapy (e.g., corticosteroids).
- Disease-specific treatments:
- Antithyroid drugs or thyroidectomy in Graves’ disease.
- Acetylcholinesterase inhibitors in myasthenia gravis.