Type III Hypersensitivity

This reaction is mediated by immune (Ag-Ab) complexes which promote tissue damage primarily through complement activation (alternate pathway). C3b as an opsonin attracts neutrophils, which then release lysosomal enzymes. C5a as a chemoattractant brings in neutrophils. Serum complement is reduced as it is used up in this process.

In the diagram above, antigen-antibody complexes are circulating and becoming trapped beneath the basement membrane of a small blood vessel, setting off the complement cascade and generating components that attract PMN's to generate an ongoing inflammatory response.

Immune complexes can be deposited systemically or locally

Systemic immune complex disease: Ag-Ab complexes form in the circulatory system and are deposited in tissues, typically near basement membranes in places such as blood vessels, glomeruli, skin, joints, pleura, and pericardium. Larger immune complexes are quickly phagocytized by macrophages and removed, but small to intermediate complexes formed with antigen excess may escape removal leading to:

  • Glomerulonephritis

  • Serum sickness

  • Vasculitis

Local immune complex disease: Also called an "Arthus" reaction, it occurs with local injection of the antigen and leads to focal vasculitis. This kind of immune reaction also plays a role in the development of hypersensitivity pneumonitis (so-called "farmer's lung").