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Hemidesmosomes, particularly those attaching epithelial cells to their basement membrane, are the tightest adhesive interactions in an animal body. This close contact, and the reinforced structure of these contacts, is crucial for the protective resilience of epithelial layers. Remember the α6β4 integrin? That would be the one that links with intermediate filaments instead of f-actin. Intermediate filaments, as we’ve already noted, are not dynamic, but about as stable as a cellular component can be. They are also very strong and are used to buttress cellular integrity. So, it is no surprise to see intermediate filaments and the α6β4 integrin playing roles in hemidesmosomes.
The distinguishing characteristic of hemidesmosomes though, is the electron-dense plaque. It can be thought of as reinforcement so that when the epithelium is stretched, the cell does not just pop loose leaving behind part of its membrane. The plaque contains several proteins, but the primary component are plectins, the linker proteins that help to bundle intermediate filaments, and connect them to each other as well as other cytoskeletal elements. Another major element of the plaques is BP230, which connects the plaque to keratin. On the extracellular side, in addition to the integrin already mentioned, there is also a transmembrane glycoprotein called BP180, which also binds to laminin elements of the basement membrane.
BP230 and BP180 are named for bullous pemphigoid, the subepidermal bullous disorder characterized by chronic blistering of the skin. It is an autoimmune disorder and in which the aberrant antibody response is to these two hemidesmosomal proteins.