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The pathogenesis of lichen planus.
A Gilhar1, T Pillar, G Winterstein
1Laboratory of Skin Research and Clinical Immunology, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.
The British Journal of Dermatology
|April 1, 1989
Summary
Lichen planus (LP) skin grafts on nude mice showed resolution of pathological changes and increased melanocytes. This suggests immune cell migration, not inherent epidermal cell changes, drives LP pathogenesis.
Area of Science:
- Dermatology
- Immunology
- Pathology
Background:
- Lichen planus (LP) exhibits characteristic epidermal changes and dermal T cells.
- The primary cause of LP, whether basal keratinocyte damage or immune-mediated destruction, remains unclear.
Purpose of the Study:
- To investigate the pathogenesis of lichen planus by examining skin grafts from affected individuals.
- To determine if inherent epidermal cell changes or immune system involvement drives LP.
Main Methods:
- Skin grafts from lichen planus patients (involved and uninvolved areas) were transplanted onto nude mice.
- Grafts were analyzed histologically and via immunofluorescence at 14 and 21 days.
- Melanocyte populations were assessed using Dopa incubation after 6 weeks.
Main Results:
- Pathological changes of lichen planus completely resolved in grafts by 21 days post-transplantation.
- An increased number of melanocytes was observed in the grafts.
- These findings suggest the immune system plays a crucial role in LP development.
Conclusions:
- The pathogenesis of lichen planus is likely not due to intrinsic epidermal cell abnormalities.
- The migration of immune system cellular elements appears to be a key factor in lichen planus development.