Type iii hypersensitivity

Definition

Type III hypersensitivity is an immune response characterized by the formation of antigen-antibody complexes that deposit in tissues, leading to inflammation and tissue damage. This type of hypersensitivity is primarily mediated by the immune system's interaction with soluble antigens, resulting in complement activation and recruitment of inflammatory cells, which can cause local tissue injury and systemic effects.

5 Must Know Facts For Your Next Test

1. In type III hypersensitivity, the antigen-antibody complexes can accumulate in various tissues, particularly in blood vessels, joints, and kidneys, leading to conditions like vasculitis and glomerulonephritis.
2. Complement activation during type III hypersensitivity contributes to inflammation by attracting neutrophils and macrophages to the site of deposition, causing further tissue damage.
3. Common examples of diseases associated with type III hypersensitivity include systemic lupus erythematosus (SLE), rheumatoid arthritis, and serum sickness.
4. The severity of type III hypersensitivity reactions can vary greatly depending on the amount of antigen present, the efficiency of immune complex clearance, and individual susceptibility.
5. Clinical manifestations can include fever, rash, joint pain, and renal issues due to the widespread effects of immune complex deposition.

Review Questions

• What role do antigen-antibody complexes play in type III hypersensitivity reactions, and how do they contribute to tissue damage?
  • Antigen-antibody complexes are central to type III hypersensitivity reactions. When soluble antigens bind with antibodies, they form these complexes that can deposit in various tissues. This deposition triggers an inflammatory response through complement activation and recruitment of immune cells like neutrophils. As these immune cells attempt to clear the complexes, they release enzymes and reactive substances that can lead to significant tissue damage.
• How does complement activation contribute to the pathology seen in diseases associated with type III hypersensitivity?
  • Complement activation plays a crucial role in the pathology of type III hypersensitivity by amplifying the inflammatory response initiated by antigen-antibody complexes. When these complexes form and deposit in tissues, they activate the complement system, leading to the release of pro-inflammatory mediators. This attracts more immune cells to the site of deposition, exacerbating inflammation and contributing to tissue injury commonly seen in conditions like systemic lupus erythematosus and rheumatoid arthritis.
• Evaluate the clinical implications of serum sickness as a manifestation of type III hypersensitivity and its management strategies.
  • Serum sickness exemplifies the clinical implications of type III hypersensitivity as it arises from an immune response to foreign proteins. Patients experience symptoms such as fever, rash, joint pain, and sometimes renal complications due to immune complex deposition. Management typically includes identifying and withdrawing the offending agent, along with supportive care like antihistamines or corticosteroids to alleviate symptoms. Understanding this condition helps in predicting potential adverse reactions following certain medical treatments involving antigens or biological agents.

Related terms

immune complex: A complex formed when antibodies bind to soluble antigens, which can lead to various immunological reactions if not effectively cleared from the body.

complement system:

A group of proteins in the blood that enhance the ability of antibodies and phagocytic cells to clear pathogens and promote inflammation.

serum sickness: A type of type III hypersensitivity reaction that occurs when antibodies form against foreign proteins introduced into the body, often following the administration of antiserum or certain medications.