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Complement and plasminogen: pathways in inflammation.

M D Kramer1, G M Hänsch, K O Rother

  • 1Institut für Immunologie und Serologie, Universität Heidelberg, Germany.

Behring Institute Mitteilungen
|April 1, 1992
PubMed
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Bullous pemphigoid involves immune reactions and the plasminogen activator system. This system

Area of Science:

  • Dermatology
  • Immunology
  • Biochemistry

Background:

  • Bullous pemphigoid is a subepidermal blistering skin disease.
  • It is characterized by autoantibodies and complement deposition at the epidermal basement membrane.
  • Proteolytic enzymes, especially plasmin, are implicated in blister formation.

Purpose of the Study:

  • To explore the interrelation between the immune reaction and the plasminogen activator system in bullous pemphigoid.
  • To elucidate the role of plasmin in subepidermal blister formation.

Main Methods:

  • The study proposes a mechanism involving complement-induced neutrophil (PMN) infiltration.
  • It suggests PMN-derived reactive oxygen species interfere with plasminogen activator inhibitors.
  • Lysosomal elastase is proposed to degrade alpha 2-antiplasmin, while urokinase-type plasminogen activator is stimulated.

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Main Results:

  • The plasmin/antiplasmin equilibrium is disturbed, leading to excess plasmin.
  • Excess plasmin degrades extracellular matrix proteins at the dermal-epidermal junction.
  • This results in epidermal-dermal dyshesion and subepidermal blister formation.

Conclusions:

  • The plasminogen activator system is a key effector system in bullous pemphigoid pathogenesis.
  • The interplay between immune response and the plasminogen activator system drives blister formation.