Pemphigus foliaceus
autoimmune blistering disease
Pemphigus foliaceus is an autoimmune blistering disease of the skin. It causes a characteristic inflammatory attack at the subcorneal layer of epidermis, which results in skin lesions that are scaly or crusted erosions with an erythematous (red) base. Mucosal involvement is absent even with widespread disease.
If there is an autoimmune IgG buildup in the epidermis, then nearly all of the antibodies are aimed against desmoglein 1. The effect of the antibodies and the immunological pathway is most likely one of three mechanisms:
Steric hindrance of the desmoglein 1: The antibody caps off the site for intracellular binding to another keratinocyte.
Activation of an endocytic pathway: The antibody activates a pathway which causes an internalization of desmogleïn 1, which in turn causes a loss of adhesion.
Disruption of function: In this case, the antibody blocks the desmoglein 1 from being formed into a desmosome. This in turn causes a loss of adhesion with acantholysis as a result.
Cause
The National Institute of Arthritis and Musculoskeletal and Skin Diseases describes the disease thus:
Normally, our immune system produces antibodies that attack viruses and harmful bacteria to keep us healthy. In people with pemphigus, however, the immune system mistakenly attacks the cells in the epidermis, or top layer of the skin, and the mucous membranes.
The public source identifies “Pemphigus foliaceus” as autoimmune blistering disease. This brief keeps that definition visible, then builds a research path around Pemphigus, foliaceus and autoimmune.
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This entry incorporates text from “Pemphigus foliaceus” on English Wikipedia. Contributors are listed in the page history. Text is available under the Creative Commons Attribution-ShareAlike 4.0 License. Selected authority identifiers and statements are retrieved from Wikidata under CC0; their references and qualifiers remain part of the verification path.