Psoriasis: dysregulation of innate immunity
J.D. Bos,
M.A. De Rie,
M.B.M. Teunissen,
G. Piskin,
J.D. Bos
Department of Dermatology, A0-235, Academic Medical Center, University of Amsterdam, P.O.Box 22700, 1100 DE Amsterdam, the Netherlands
Search for more papers by this authorM.A. De Rie
Department of Dermatology, A0-235, Academic Medical Center, University of Amsterdam, P.O.Box 22700, 1100 DE Amsterdam, the Netherlands
Search for more papers by this authorM.B.M. Teunissen
Department of Dermatology, A0-235, Academic Medical Center, University of Amsterdam, P.O.Box 22700, 1100 DE Amsterdam, the Netherlands
Search for more papers by this authorG. Piskin
Department of Dermatology, A0-235, Academic Medical Center, University of Amsterdam, P.O.Box 22700, 1100 DE Amsterdam, the Netherlands
Search for more papers by this authorJ.D. Bos,
M.A. De Rie,
M.B.M. Teunissen,
G. Piskin,
J.D. Bos
Department of Dermatology, A0-235, Academic Medical Center, University of Amsterdam, P.O.Box 22700, 1100 DE Amsterdam, the Netherlands
Search for more papers by this authorM.A. De Rie
Department of Dermatology, A0-235, Academic Medical Center, University of Amsterdam, P.O.Box 22700, 1100 DE Amsterdam, the Netherlands
Search for more papers by this authorM.B.M. Teunissen
Department of Dermatology, A0-235, Academic Medical Center, University of Amsterdam, P.O.Box 22700, 1100 DE Amsterdam, the Netherlands
Search for more papers by this authorG. Piskin
Department of Dermatology, A0-235, Academic Medical Center, University of Amsterdam, P.O.Box 22700, 1100 DE Amsterdam, the Netherlands
Search for more papers by this authorJan D. Bos MD, PhD, FRCP, Professor and Chairman.
E-mail: [email protected]
Conflicts of interest: None declared.
Summary
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.
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