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Ultrastructural findings in bullous pemphigoid
Journal of Cutaneous Pathology
|January 1, 1975
Summary
Bullous pemphigoid blisters form by basal cell separation, leaving the basal lamina intact. Skin surrounding blisters shows widened intercellular spaces and fewer half-desmosomes, a change also induced by xenon lamp irradiation.
Area of Science:
- Dermatology
- Immunodermatology
- Electron Microscopy
Background:
- Bullous pemphigoid (BP) is an autoimmune blistering disease of the skin.
- Understanding the ultrastructural and immunopathological changes in BP is crucial for diagnosis and treatment.
- The precise mechanism of blister formation and the role of perilesional skin changes require further investigation.
Purpose of the Study:
- To investigate the ultrastructural and immunofluorescence characteristics of blister formation in bullous pemphigoid.
- To compare changes in perilesional skin, distant normal skin, and artificially induced lesions.
- To elucidate the cellular and molecular events underlying blister formation in BP.
Main Methods:
- Electron microscopy and direct immunofluorescence examinations were performed.
- Skin samples included blister borders, perilesional normal skin, distant normal skin, and skin subjected to xenon lamp irradiation.
- Analysis focused on cellular morphology, intercellular spaces, and the presence of immunoglobulins and complement.
Main Results:
- Bullous pemphigoid blisters result from cleavage of basal cells from an intact basal lamina.
- Perilesional skin exhibits widened intercellular spaces and a reduced number of half-desmosomes.
- Xenon lamp irradiation induced similar ultrastructural changes to perilesional skin, but without in vivo immunoglobulin and complement deposition.
Conclusions:
- The findings elucidate the specific cleavage plane in bullous pemphigoid blisters.
- Perilesional skin changes in BP are characterized by alterations in cell adhesion structures.
- Xenon lamp irradiation can mimic some ultrastructural features of perilesional skin in BP, suggesting a role for external stimuli in disease pathogenesis.