Korean J Dermatol.  1988 Jun;26(3):292-297.

Plasmin and Its Inhibitors in the Lesional Skin of Pemphigus

Abstract

The exact pathomechanism of anti-epidermal cell pemphigus antibodies in developing acantholytic changes is unknown. Recent investigations have suggested that pemphigus antibodies, after binding to the antigenic site, induce activation of epidermal plasminogen activator. This increased activity of the plasminogen activator converts plasminogen to plasmin in high level degrades intercellular bridges resulting in loss of adhesion between epidermal cells. Author examined, by modified direct immunofluorescence, the deposition of plasmin and its inhibitor proteins such as alpha 1-antitrypsin and alpha 2-macroglobulin, with the early lesional skin specimens from 5 patients of pemphigus All these lesional skin demonstrated intense deposits of plasmin and aIpha 2-mscrogIobulin, and to a less degree alpha l-antitrypsin, all having indentical patterns to that of IgGautoantibodies. These proteins were also stained at the dermoepidermal junction and upper dermis, but less intensely. The identification of these particular proteins ; plasmin, alpha 1 antitrypsin, and alpha 2 macroglobulin, could be an alternate mean for the enzyme-histologic diagncsis of pemphigus.


MeSH Terms

alpha 1-Antitrypsin
alpha-Macroglobulins
Antibodies
Dermis
Fibrinolysin*
Fluorescent Antibody Technique, Direct
Humans
Pemphigus*
Plasminogen
Plasminogen Activators
Skin*
Antibodies
Fibrinolysin
Plasminogen
Plasminogen Activators
alpha 1-Antitrypsin
alpha-Macroglobulins
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