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Glucocorticoids: The mode of action in bullous pemphigoid
Author(s) -
Kubin Minna E.,
Hellberg Lars,
Palatsi Riitta
Publication year - 2017
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13408
Subject(s) - bullous pemphigoid , autoantibody , immune system , glucocorticoid receptor , immunology , glucocorticoid , pemphigoid , receptor , inflammation , innate immune system , antibody , chemistry , medicine
Bullous pemphigoid ( BP ) is the most common of pemphigoid diseases caused by autoantibodies against the structures of dermoepidermal junction followed by complement activation, innate immune cell infiltration, neutrophil proteinase secretion and subepidermal blister formation. The first‐line treatment of BP is topical and systemic glucocorticoids ( GC ). Regulation of the immune system and inflammatory cells is the main target of GC actions. GC s act through genomic and non‐genomic mechanisms. The human glucocorticoid receptor ( GR ) mediates most of the biologic effects of GC: cytosolic GR binds GC s and is capable to bind to glucocorticoid response elements in DNA and either transactivate or transrepress genes depending on the tissue and cell type. In addition, GR exerts rapid, non‐genomic effects possibly mediated by membrane‐localized receptors or by translocation to mitochondria. GC s can also interact directly with several enzymes and cytokines. As a target treatment for BP , the production of autoantibodies should be discontinued. GC s, in spite of their wide immunosuppressive actions, are weak to stop immunoglobulin G (IgG) autoantibody formation. However, both systemic and topical GC s are able to reduce the clinical symptoms of BP . GC s are used to inhibit the secondary inflammation and symptoms, such as blistering and pruritus, and it is shown that GC treatment will gradually decrease also the autoantibody formation. Our review article analyses the mode of action of GC treatment in BP , as far it is possible due to paucity of modern immunological studies.