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Type III HS (Immune Complex Mediated) 

  • Induced by Ag-Ab complexes that produce Q tissue damage as a result of their capacity to activate the
  • complement systems    a. Circulatory I/C     b. In situ I/C (immune compltes)
  • Exogenous Ag - Bacterial/virus/fungi/ parasite drug/ heroin. Quinine
  • Endogenous Ag → a. Nuclear Ag: SLE    b. Immunoglobulins: Rheumatoid arthritis
  • Tumor antigens: Glomerulonephritis
  • Generalized / e.g.:
  • Acute Serum Sickness (After administration of large amounts of horse anti-tetanus serum
  • Localized (e.g. local arthus reaction) 

  1. Phase I
    Immune Complex Formation
    1. Ab. Produced approx. 5 days after introduction of Ag
    2. Large antigen / Ab. complexes - rapidly removed by macrophages. Most pathogenic are small/ intermediate complexes
  2. Phase II
    Immune complex deposition Q
  1. Phase III
Complex mediated inflammation seen 10 days after antigen administration and causes Vasculitis, glomerulonephritis and arthritis­ Q

Disease Antigen Involved Clinicopathologic Manifestations
SLE Nuclear antigens Nephritis, skin lesions, arthritis, others
Poststreptococcal GN Streptococcal cell wall antigen(s); may be "planted" in glomerular basement membrane Nephritis
PAN Hepatitis B virus antigen Systemic vasculitis
Reactive arthritis Bacterial antigens (Yersinia) Acute arthritis
Serum sickness Various proteins, such as foreign serum protein (horse anti-thymocyte globulin) Arthritis, vasculitis, nephritis
Arthus reaction (experimental) Various foreign proteins Cutaneous vasculitis

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