Possible Derivation of Cutaneous Amyloid from Degenerating Collagen Fibers: Ultrastructural, Immunohistological Studies Employing Anticollagen Antibodies
It has been suggested for some years that the cutaneous fibroblasts are the most probable sythesizer in the primary cutaneous amyloidoses(1, 2,3,4,5). However, nowadays, increasing number of investigators have suggested that amyloid in the primary cutaneous amyloidoses originates from necrotizing keratinocytes(6,7,8,9,10). Black & Wilson Jones (6) first reported this possibility from the light microscopic observation. This view has been supported by the reports of ‘colloid-amyloid body’ as the possible precursor amyloid (7) and positive reaction of amyloid with antikeratin antibodies using immunofluorescence microscopy and immunoelectron microscopy (8,9). Investigations employed several monoclonal anti-keratin antibodies were performed by Eto et al. (10) and they observed only one of them reacts with cutaneous amyloid in the primary cutaneous amyloidoses. However, several unsolved questions for this theory might be pointed out. In the monoclonal experiments, several antibodies which reacted with whole epidermis could not: react with amyloid masses and it is unclear how the significant ‘colloid-amyloid body’ were stained with these monoclonal antibodies which were positive for colloid bodies whereas negative for amyloid. It is also difficult to explain why many colloid bodies which are frequently observed in the cutaneous disorders,for example, lichen planus or discoid lupus erythematosus do rot change into amyloid masses. In addition, we and Noren et al. (11,12) have reported that in some cases of primary cutaneous amyloidoses, anti-keratin investigation is negative for amyloid deposition.
KeywordsDiscoid Lupus Erythematosus Collagen Antibody Conventional Electron Microscopy Antikeratin Antibody Lichen Amyloidosus
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