The pathophysiological role of cytokines in psoriasis

(c) 1999 Prous Science. All rights reserved..

Psoriasis is a chronic inflammatory cutaneous disorder. Recent data indicate that T cells and cytokines are of major importance in the pathophysiology of this frequent immune disease. The cutaneous and systemic overexpression of several proinflammatory cytokines, particularly type-1 cytokines such as IL-2, IL-6, IL-8, IL-12, IFN-gamma and TNF-alpha, has been demonstrated. The overexpression of these proinflammatory cytokines is considered to be responsible for initiation, maintenance and recurrence of skin lesions. The cellular composition of the inflammatory infiltrate within the plaques as well as the keratinocyte hyperproliferation appears to be directed by cytokines as well. Thus, the overexpression of the chemoattractant IL-8 contributes to the accumulation of granulocytes, a characteristic finding in psoriatic lesions. In contrast to the overexpression of proinflammatory cytokines, a relatively low level of expression of the antiinflammatory cytokines IL-1RA and IL-10 has been found, suggesting an insufficient counterregulatory capacity in psoriasis which might have a genetic background. The new pathophysiologic understanding of psoriasis offers the opportunity for well-targeted therapeutic interventions which should be more effective and better tolerated than the approaches used thus far. In fact, the cytokine imbalance represents an interesting target. This is supported by the therapeutic effects of IL-10, a type-2 cytokine with major influence on immunoregulation, since it inhibits type-1/proinflammatory cytokine formation.

Medienart:

Artikel

Erscheinungsjahr:

1999

Erschienen:

1999

Enthalten in:

Zur Gesamtaufnahme - volume:35

Enthalten in:

Drugs of today (Barcelona, Spain : 1998) - 35(1999), 12 vom: 13. Dez., Seite 913-24

Sprache:

Englisch

Beteiligte Personen:

Asadullah, K [VerfasserIn]
Döcke, W D [VerfasserIn]
Volk, H D [VerfasserIn]
Sterry, W [VerfasserIn]

Themen:

Journal Article

Anmerkungen:

Date Completed 24.10.2003

Date Revised 08.04.2022

published: Print

Citation Status PubMed-not-MEDLINE

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM127204121