Glucocorticoids : the mode of action in bullous pemphigoid
|Author:||Kubin, Minna E.1; Hellberg, Lars2; Palatsi, Riitta1|
1PEDEGO Research Unit, Oulu Center for Cell-Matrix Research, Department of Dermatology and Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland
2Institute for Medical Microbiology and Hygiene, University of Lübeck, Lübeck, Germany
|Online Access:||PDF Full Text (PDF, 0.2 MB)|
|Persistent link:|| http://urn.fi/urn:nbn:fi-fe2019103135996
John Wiley & Sons,
|Publish Date:|| 2019-10-31
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. GCs act through genomic and non‐genomic mechanisms. The human glucocorticoid receptor (GR) mediates most of the biologic effects of GC: cytosolic GR binds GCs 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. GCs can also interact directly with several enzymes and cytokines. As a target treatment for BP, the production of autoantibodies should be discontinued. GCs, in spite of their wide immunosuppressive actions, are weak to stop immunoglobulin G (IgG) autoantibody formation. However, both systemic and topical GCs are able to reduce the clinical symptoms of BP. GCs 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.
|Pages:||1253 - 1260|
|Type of Publication:||
A2 Review article in a scientific journal
|Field of Science:||
3121 General medicine, internal medicine and other clinical medicine
© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. This is the peer reviewed version of the following article: Kubin, ME, Hellberg, L, Palatsi, R. Glucocorticoids: The mode of action in bullous pemphigoid. Exp Dermatol. 2017; 26: 1253– 1260. https://doi.org/10.1111/exd.13408, which has been published in final form at https://doi.org/10.1111/exd.13408. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.