Type III hypersensitivity

Type III Hypersensitivity

Diagram illustrating immune complex formation

Type III hypersensitivity, also known as immune complex-mediated hypersensitivity, is a form of hypersensitivity reaction that involves the formation of immune complexes. These complexes are formed when antibodies bind to soluble antigens in the blood. The immune complexes can deposit in various tissues, leading to inflammation and tissue damage. This type of hypersensitivity is distinct from Type I hypersensitivity, which involves IgE antibodies and immediate allergic reactions, and Type II hypersensitivity, which involves antibody-mediated destruction of cells.

Mechanism

The mechanism of Type III hypersensitivity involves several key steps:

1. Formation of Immune Complexes: When antigens enter the bloodstream, they can bind to specific antibodies, forming antigen-antibody complexes. These are known as immune complexes.

2. Deposition in Tissues: The immune complexes can circulate in the bloodstream and become deposited in various tissues, such as the kidneys, joints, and blood vessels.

3. Activation of Complement System: The deposited immune complexes activate the complement system, a part of the immune system that enhances the ability to clear microbes and damaged cells.

4. Inflammatory Response: Activation of the complement system leads to the recruitment of inflammatory cells, such as neutrophils, to the site of deposition. These cells release enzymes and reactive oxygen species that cause tissue damage.

5. Tissue Damage: The inflammation and release of enzymes result in tissue damage, which can manifest as various clinical symptoms depending on the site of immune complex deposition.

Clinical Manifestations

Type III hypersensitivity reactions can lead to a variety of clinical conditions, depending on where the immune complexes are deposited:

- Systemic lupus erythematosus (SLE): In SLE, immune complexes are deposited in the kidneys, skin, and other organs, leading to a wide range of symptoms.

- Rheumatoid arthritis: In this condition, immune complexes are deposited in the joints, causing inflammation and joint damage.

- Post-streptococcal glomerulonephritis: Following a streptococcal infection, immune complexes can deposit in the kidneys, leading to inflammation and impaired kidney function.

- Henoch-Schönlein purpura: This condition involves the deposition of IgA immune complexes in small blood vessels, leading to a purpuric rash, abdominal pain, and kidney involvement.

IgA immunostaining in Henoch-Schönlein purpura

Diagnosis

Diagnosis of Type III hypersensitivity involves clinical evaluation and laboratory tests. Tests may include:

- Detection of Immune Complexes: Laboratory tests can detect circulating immune complexes in the blood.

- Complement Levels: Low levels of complement proteins in the blood can indicate activation of the complement system.

- Biopsy: Tissue biopsy can reveal immune complex deposition and inflammation.

Treatment

Treatment of Type III hypersensitivity focuses on reducing inflammation and preventing further immune complex formation. Common treatments include:

- Corticosteroids: These drugs reduce inflammation and immune response.

- Immunosuppressive Agents: Drugs such as cyclophosphamide and azathioprine can suppress the immune system.

- Plasmapheresis: This procedure removes immune complexes from the blood.

Related Pages

- Hypersensitivity - Immune system - Autoimmune disease