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Pathogenesis of psoriasis
1Department of Medicine, University of Utah Health Sciences Center, Salt Lake City 84132, USA.
Dermatologic Clinics
|October 1, 1995
Summary
Psoriatic skin cells have a genetic defect causing hyperproliferation and altered differentiation, leading to disease expression when regulatory signals are overwhelmed. This framework hypothesis explains psoriasis pathogenesis through complex cellular and genetic interactions.
Area of Science:
- Dermatology
- Immunology
- Genetics
Background:
- Psoriasis pathogenesis involves complex interactions between epidermal, dermal, and immune cells.
- Keratinocytes in psoriatic patients exhibit unique hyperproliferation and altered differentiation capabilities.
Purpose of the Study:
- To support the framework hypothesis of psoriasis.
- To elucidate the genetic underpinnings of psoriatic phenotype expression.
- To explore the role of gene regulation in psoriasis development.
Main Methods:
- Analysis of cellular interactions in psoriatic skin.
- Investigation of cytokine and growth factor profiles.
- Postulation of genetic defects in regulatory elements controlling proliferation.
Main Results:
- Psoriatic keratinocytes show inherent hyperproliferative and altered differentiation capacity.
- Genetic aberrations are postulated to be proximal to inflammatory cascade initiation.
- Defects in transcription regulatory elements or related genes can lead to psoriatic lesions.
Conclusions:
- The entire epidermis of individuals with a psoriatic phenotype can express disease.
- Control of disease expression involves intricate interactions of cellular and humoral elements.
- Genetic defects affecting gene regulation, receptor/ligand binding, or cytokine pathways contribute to psoriasis development and resistance to therapies.