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Neueste Aspekte in der Pathogenese der Psoriasis

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Zusammenfassung

In den letzten Jahren hat ein Paradigmenwechsel im Verständnis der Pathogenese der Psoriasis stattgefunden. Psoriasis wird nun als eine in weiten Bereichen T-Zell-induzierte Hautentzündung angesehen. Genetische Prädisposition und mikrobielle Umwelt wirken bei der Auslösung einer antigenspezifischen T-Zell-vermittelten Immunreaktion in der Haut zusammen, welche nach ihrem Ausbruch oft lebenslang persistiert. Der Phänotyp der psoriatischen Entzündung wird hierbei durch die funktionelle Differenzierung der pathogenen T-Zellen bestimmt. Durch den Fortschritt im Verständnis der Psoriasispathogenese wurden T-Zellen und ihre Zytokine zu Ansatzpunkten für die Entwicklung kausaler Behandlungsansätze, welche die Psoriasistherapie in naher Zukunft entscheidend verändern werden.

Abstract

During recent years the understanding of psoriasis pathogenesis has changed essentially. Psoriasis is now considered as a T cell mediated inflammation of the skin. Genetic predisposition and microbial environment cooperate in the induction of an antigen-specific T cell mediated immune response which may persist lifelong. The phenotype of the psoriatic inflammation is determined by the particular functional differentiation of the pathogenic T cells. The progress in understanding the pathogenesis of psoriasis has identified T cells and T cell-derived cytokines as targets for causal treatment approaches that in the near future will change psoriasis therapy considerably.

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Literatur

  1. Albert LJ, Inman RD (1999) Molecular mimicry and autoimmunity. N Engl J Med 341:2068–2074

    Google Scholar 

  2. Asadullah K, Sterry W, Stephanek K et al. (1998) IL-10 is a key cytokine in psoriasis. Proof of principle by IL-10 therapy: a new therapeutic approach. J Clin Invest 101:783–794

    Google Scholar 

  3. Baker BS, Bolith S, Powles AV et al. (1992) Streptococcal antigen-specific T lymphocytes in skin lesions of guttate psoriasis. J Invest Dermatol 98:535–538

    Google Scholar 

  4. Casanova JL, Maryanski JL (1993) Antigen-selected T-cell receptor diversity and self-nonself homology. Immunol Today 14:391–394

    Google Scholar 

  5. Chang JCC, Smith LR, Froning KJ et al. (1994) CD8+ T cells in psoriatic lesions preferentially use T-cell receptor Vβ3 and/orVβ13.1 genes. Proc Natl Acad Sci USA 91:9282–9286

    Google Scholar 

  6. Ellis CN, Krueger GG (2001) Treatment of chronic plaque psoriasis by selective targeting of memory effector T lymphocytes. N Engl J Med;345:248–255

    Google Scholar 

  7. Ghoreschi K, Thomas P, Breit S et al. (in press) Interleukin-4 therapy of psoriasis induces TH2 responses and improves human autoimmune disease. Nature Med

  8. Gudmundsdottir AS, Sigmundsdottir H, Sigurgeirsson B et al. (1999) Is an epitope on keratin 17 a major target for autoreactive T lymphocytes in psoriasis? Clin Exp Immunol 117:580–586

    Google Scholar 

  9. Guedjonsson JE, Karason A, Antonsdottir AA et al. (2002) HLA-Cw6-positive and HLA-Cw6-negative patients with psoriasis vulgaris have distinct clinical features. J Invest Dermatol 118:362–365

    Google Scholar 

  10. Henseler T, Christophers E (1985) Psoriasis of early and late onset: characterization of two types of psoriasis vulgaris. J Am Acad Dermatol 13:450–456

    Google Scholar 

  11. Mallon E, Bunce M, Savoie H et al. (2000) HLA-C and guttate psoriasis. Br J Dermatol 143:1177–1182

    Google Scholar 

  12. Menssen A, Trommler P, Vollmer S et al. (1995) Evidence for an antigen-specific cellular immune response in skin lesions of patients with psoriasis vulgaris. J Immunol 155:4078–4083

    Google Scholar 

  13. Nair RP, Henseler T, Jenisch S et al. (1997) Evidence for two psoriasis susceptibility loci (HLA and 17q) and two novel candidate regions (16q and 20p) by genome-wide scan. Hum Mol Genet 6:1349–1356

    Google Scholar 

  14. Nyfors A, Rasmussen PA, Lemholt K, Eriksen B (1975) Improvement of refractory psoriasis vulgaris after tonsillectomy. Dermatologica 151:216–222

    Google Scholar 

  15. Prinz JC (2001) Psoriasis vulgaris—a sterile antibacterial skin reaction mediated by cross-reactive T cells? An immunological view of the pathophysiology of psoriasis. Clin Exp Dermatol 26:326–332

    Google Scholar 

  16. Prinz JC (in press) The role of T cells in psoriasis. J Eur Ac Derm Venerol

  17. Prinz JC, Braun-Falco O, Meurer M et al. (1991) Chimeric CD4 monoclonal antibody in the treatment of generalized pustular psoriasis. Lancet 338:320–321

    Google Scholar 

  18. Prinz JC, Gross B, Vollmer S et al. (1994) T cell clones from psoriasis skin lesions can promote keratinocyte proliferation in vitro. Eur J Immunol 24:593–598

    Google Scholar 

  19. Prinz JC, Vollmer S, Boehncke WH et al. (1999) Selection of conserved TCR-VDJ-rearrangements in chronic psoriatic plaques indicates a common antigen in psoriasis vulgaris. Eur J Immunol 29:3360–3368

    Google Scholar 

  20. Robinson JH, Kehoe MA (1992) Group A streptococcal M proteins: virulence factors and protective antigens. Immunol Today 13:362–367

    Google Scholar 

  21. Said Nahal R, Miceli Richard C et al. (2001) Phenotypic diversity is not determined by independent genetic factors in familial spondylarthropathy. Arthritis Rheum 45:478–484

    Google Scholar 

  22. Schmitt Egenolf M, Eiermann TH et al. (1996) Familial juvenile onset psoriasis is associated with the human leukocyte antigen (HLA) class I side of the extended haplotype Cw6-B57-DRB1*0701-DQA1*0201-DQB1*0303: a population- and family-based study. J Invest Dermatol 106:711–714

    Google Scholar 

  23. Sigmundsdottir H, Sigurgeirsson B, Troye Blomberg M et al. (1997) Circulating T cells of patients with active psoriasis respond to streptococcal M-peptides sharing sequences with human epidermal keratins. Scand J Immunol 45:688–697

    Google Scholar 

  24. Trembath RC, Clough RL, Rosbotham JL et al. (1997) Identification of a major susceptibility locus on chromosome 6p and evidence for further disease loci revealed by a two stage genome-wide search in psoriasis. Hum Mol Genet 6:813–820

    Google Scholar 

  25. Valdimarsson H, Baker BS, Jonsdottir I et al. (1995) Psoriasis: a T-cell-mediated autoimmune disease induced by streptococcal superantigens? Immunol Today 16:145–149

    Google Scholar 

  26. Vollmer S, Menssen A, Prinz JC (2001) Dominant lesional T cell receptor rearrangements persist in relapsing psoriasis but are absent from nonlesional skin: evidence for a stable antigen-specific pathogenic T cell response in psoriasis vulgaris. J Invest Dermatol 117:1296–1301

    Google Scholar 

  27. Vollmer S, Menssen A, Trommler P et al. (1994) T lymphocytes derived from skin lesions of patients with psoriasis vulgaris express a novel cytokine pattern that is distinct from that of T helper type 1 and T helper type 2 cells. Eur J Immunol 24:2377–2382

    Google Scholar 

  28. Weisenseel P, Laumbacher B, Besgen P et al. (2002) Streptococcal infection distinguishes different types of psoriasis. J Med Genet 39:767–768

    Google Scholar 

  29. Wrone Smith T, Nickoloff BJ (1996) Dermal injection of immunocytes induces psoriasis. J Clin Invest 98:1878–1887

    Google Scholar 

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Correspondence to Jörg C. Prinz.

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Prinz, J.C. Neueste Aspekte in der Pathogenese der Psoriasis. Hautarzt 54, 209–214 (2003). https://doi.org/10.1007/s00105-003-0490-9

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