[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.
Bos
W E M
WE
Erasmus MC, afd. Dermatologie en Venereologie, Postbus 2040, 3000 CA Rotterdam.
Thio
H B
HB
Neumann
H A M
HA
van der Fits
L
L
Prens
E P
EP
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