Conflicts of interest: None declared.
Psoriasis: dysregulation of innate immunity
Version of Record online: 22 JUN 2005
British Journal of Dermatology
Volume 152, Issue 6, pages 1098–1107, June 2005
How to Cite
Bos, J.D., De Rie, M.A., Teunissen, M.B.M. and Piskin, G. (2005), Psoriasis: dysregulation of innate immunity. British Journal of Dermatology, 152: 1098–1107. doi: 10.1111/j.1365-2133.2005.06645.x
- Issue online: 22 JUN 2005
- Version of Record online: 22 JUN 2005
- Accepted for publication 25 December 2004
- cytokine production;
- NK T cell;
- specific immunity;
- T-cell activation;
- type 1 T cell
The current understanding of the function of natural killer (NK) T cells in innate immunity and their potential to control acquired specific immunity, as well as the remarkable efficacy of antitumour necrosis factor-α biological treatments in psoriasis, forces us to refine the current T-cell hypothesis of psoriasis pathogenesis, and to give credit to the role of innate immunity. Psoriasis might be envisioned to be a genetically determined triggered state of otherwise dormant innate immunity. This aggravated state of innate immunity is represented by the activity of NK T cells, dendritic cells, neutrophils and keratinocytes, leading to the recruitment and activation of preferentially type 1 T cells, possibly in an antigen-independent way. Keratinocytes in psoriasis then are sensitive to the effects of T-cell activation and cytokine production, interferon (IFN)-γ, by responding with psoriasiform hyperplasia. The chronic inflammation of psoriatic lesions suggests that this might be due to a deficiency in downregulation processes (e.g. a defect in the regulatory T-cell repertoire) and/or the persistence of an unknown trigger resulting in an exaggerated innate immune response.