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Psoriasis is the outcome of a skin cells anomaly

[|Since psoriasis is a polygenic disease, it cannot be the outcome of a
single cell anomaly – again, here I disagree strongly.|auteur195]

[|I strongly support the statement "psoriasis
is the outcome of a skin cell anomaly". Indeed, we cannot consider psoriasis a
defect in one cell type. Although T-cells have received a lot of attention, it
is intriguing that anti-TNFa
treatments are more effective as compared to T-cell specific approaches. It is
the broad interaction of TNF-a which
proves to be essential for a substantial therapeutic effect, whilst T-cell
targeted treatments have a more modest efficacy.|auteur197]

It has been clearly demonstrated for over 30 years now, particularly by Gerald Krueger, that grafting lesional or non lesional psoriatic skin onto a nude mouse ends in maintaining a psoriatic phenotype in the form of persistent epidermal hyperproliferation, when comparing these grafts with normal skin grafts. This epidermal hyperproliferation is only produced if the dermis is also grafted, indicating that dermal cells are necessary for the expression of a psoriatic phenotype. More recently, it has been shown that activated T lymphocytes from a psoriasis plaque, when injected into a psoriatic skin grafted onto a nude mouse, led to the appearance of a clinical and histological psoriasis plaque. By contrast, injecting these same cells into normal skin grafted onto the nude mouse does not have this effect. The inflammatory cells, therefore, only cause psoriasis to appear if they encounter abnormal skin cells.

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