[The pathogenesis of inflammatory dermatoses, especially psoriasis].
The skin contains a variety of cell types and mediators, which together constitute the skin's immune system and play a key role in protecting the human body against dangers from outside. Dysregulation of the skin's immune system, however, frequently occurs and can result in undesirable inflammatory processes in the skin. A typical example of an undesirable inflammation in the skin is the chronic inflammatory skin disease psoriasis. In the pathogenesis of psoriasis, both genetic and environmental factors play a key role. In psoriasis, the complex interactions between T-lymphocytes, antigen-presenting cells, keratinocytes and pro-inflammatory cytokines and chemokines are disturbed. The two most widely accepted hypotheses are: (a) psoriasis is a T-cell mediated autoimmune disease, and (b) psoriasis is the result of a too finely adjusted system for regulating inflammation in the skin. The result of both mechanisms is a chronic inflammatory reaction fuelled by pro-inflammatory type-I cytokines that lead to the psoriasis-skin phenotype. With the development ofbiologicals, it has become feasible to target specific molecules in the immune process, for example type-I cytokines and the molecules present on pathogenic T-cells. This approach has already proved successful in the treatment of rheumatoid arthritis and Crohn's disease, creating novel therapeutic options for psoriasis and other inflammatory dermatoses.
Erasmus MC, afd. Dermatologie en Venereologie, Postbus 2040, 3000 CA Rotterdam.
W E M
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Bos
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Thio
H A M
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Neumann
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L
van der Fits
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Prens
D001323:Autoantibodies / Q000097:blood; D016207:Cytokines / Q000276:immunology*; D005786:Gene Expression Regulation; D020022:Genetic Predisposition to Disease; D006801:Humans; D011565:Psoriasis / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000473:pathology
D001323:Autoantibodies; D016207:Cytokines