Pathogenese van inflammatoire dermatosen, in het bijzonder 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-1 cytokines that lead to the psoriasis-skin phenotype.

- With the development of biologicals, it has become feasible to target specific molecules in the immune process, for example type-1 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.

Ned Tijdschr Geneeskd. 2006;150:179-83