Pathogenesis and therapy of psoriasis

Nature

Volumn 445, Issue 7130, 2007, Pages 866-873

  Lowes, Michelle A ^a   Bowcock, Anne M ^b   Krueger, James G ^a  

^a ROCKEFELLER UNIVERSITY   (United States)

^b WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ABATACEPT; ABT 874; ADALIMUMAB; ALEFACEPT; BASILIXIMAB; CENT 1275; CYCLOSPORIN; CYCLOSPORIN A; DACLIZUMAB; DENILEUKIN DIFTITOX; EFALIZUMAB; ETANERCEPT; FUMARIC ACID DERIVATIVE; INFLIXIMAB; METHOTREXATE; MONOCLONAL ANTIBODY; PIMECROLIMUS; PROTEIN INHIBITOR; TACROLIMUS; UNCLASSIFIED DRUG; ZENEPAX;

DISEASE TREATMENT; IMMUNE SYSTEM; PATHOGENICITY; PROTEIN; SKIN DISORDER;

BIOENGINEERING; BIOLOGICAL MODEL; CLINICAL TRIAL; HEREDITY; HUMAN; NONHUMAN; PRIORITY JOURNAL; PROTEIN INTERACTION; PSORIASIS; REVIEW;

EID: 33847279025     PISSN: 00280836     EISSN: 14764687     Source Type: Journal    
DOI: 10.1038/nature05663     Document Type: Review

References (66)

1. Krueger, J. G. The immunologic basis for the treatment of psoriasis with new biologic agents. J. Am. Acad. Dermatol. 46, 1-23 (2002).
2. Lebwohl, M. Psoriasis. Lancet 361, 1197-1204 (2003).
3. Nickoloff, B. J. & Nestle, F. O. Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities. J. Clin. Invest. 113, 1664-1675 (2004).
4. Bowcock, A. M. & Krueger, J. G. Getting under the skin: the immunogenetics of psoriasis. Nature Rev. Immunol. 5, 699-711 (2005).
5. Schon, M. P. & Boehncke, W. H. Psoriasis. N. Engl. J. Med. 352, 1899-1912 (2005).
6. Gaspari, A. A. Innate and adaptive immunity and the pathophysiology of psoriasis. J. Am. Acad. Dermatol. 54, S67-S80 (2006).
7. Davidson, A. & Diamond, B. Autoimmune diseases. N. Engl. J. Med. 345, 340-350 (2001).
8. Liu, Y., Krueger, J. G. & Bowcock, A. M. Psoriasis: genetic associations and immune system changes. Genes Immunity advance online publication (9 November 2006) doi:10.1038/sj.gene.6364351.
9. Christensen, T. E. et al. Observations of psoriasis in the absence of therapeutic intervention identifies two unappreciated morphologic variants, thin-plaque and thick-plaque psoriasis, and their associated phenotypes. J. Invest. Dermatol. 126, 2397-2403 (2006).
10. Lew, W., Lee, E. & Krueger, J. G. Psoriasis genomics: analysis of proinflammatory (type 1) gene expression in large plaque (Western) and small plaque (Asian) psoriasis vulgaris. Br. J. Dermatol. 150, 668-676 (2004).
11. Clark, R. A. et al. The vast majority of CLA+ T cells are resident in normal skin. J. Immunol. 176, 4431-4439 (2006).
12. Boyman, O. et al. Activation of dendritic antigen-presenting cells expressing common heat shock protein receptor CD91 during induction of psoriasis. Br. J. Dermatol. 152, 1211-1218 (2005).
13. Boyman, O. et al. Spontaneous development of psoriasis in a new animal model shows an essential role for resident T cells and tumor necrosis factor-?. J. Exp. Med. 199, 731-736 (2004).
14. Lew, W., Bowcock, A. M. & Krueger, J. G. Psoriasis vulgaris: cutaneous lymphoid tissue supports T-cell activation and 'Type 1' inflammatory gene expression. Trends Immunol. 25, 295-305 (2004).
15. Nestle, F. O. et al. Plasmacytoid predendritic cells initiate psoriasis through interferon-alpha production. J. Exp. Med. 202, 135-143 (2005).
16. Lowes, M. A. et al. Increase in TNF-? and inducible nitric oxide synthase-expressing dendritic cells in psoriasis and reduction with efalizumab (anti-CD11a). Proc. Natl Acad. Sci. USA 102, 19057-19062 (2005).
17. Larrengina, A. T. & Falo, L. D. Changing paradigms in cutaneous immunology: adapting with dendritic cells. J. Invest. Dermatol. 124, 1-12 (2005).
18. Serbina, N. V., Salazar-Mather, T. P., Biron, C. A., Kuziel, W. A. & Pamer, E. G. TNF/iNOS-producing dendritic cells mediate innate immune defense against bacterial infection. Immunity 19, 59-70 (2003).
19. Lee, E. et al. Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris. J. Exp. Med. 199, 125-130 (2004).
20. + myeloid-derived cells in psoriasis: gene regulation and cellular effects. J. Invest. Dermatol. 126, 1590-1599 (2006).
21. Zhou, X. et al. Novel mechanisms of T-cell and dendritic cell activation revealed by profiling of psoriasis on the 63,100-element oligonucleotide array. Physiol. Genomics 13, 69-78 (2003).
22. Weninger, W. et al. Naive T cell recruitment to nonlymphoid tissues: a role for endothelium-expressed CC chemokine ligand 21 in autoimmune disease and lymphoid neogenesis. J. Immunol. 170, 4638-4648 (2003).
23. Weninger, W. & von Andrian, U. H. Chemokine regulation of naive T cell traffic in health and disease. Semin. Immunol. 15, 257-270 (2003).
24. McKenzie, B. S., Kastelein, R. A. & Cua, D. J. Understanding the IL-23-IL-17 immune pathway. Trends Immunol. 27, 17-23 (2006).
25. Nickoloff, B. J., Bonish, B., Huang, B. B. & Porcelli, S. A. Characterization of a T cell line bearing natural killer receptors and capable of creating psoriasis in a SCID mouse model system. J. Dermatol. Sci. 24, 212-225 (2000).
26. Prinz, J. C. et al. T cell clones from psoriasis skin lesions can promote keratinocyte proliferation in vitro via secreted products. Eur. J. Immunol. 24, 593-598 (1994).
27. high regulatory T cells in psoriasis: mechanism underlying unrestrained pathogenic effector T cell proliferation. J. Immunol. 174, 164-173 (2005).
28. Gottlieb, S. L. et al. Response of psoriasis to a lymphocyte-selective toxin (DAB389IL-2) suggests a primary immune, but not keratinocyte, pathogenic basis. Nature Med. 1, 442-447 (1995).
29. Abrams, J. R. et al. CTLA4Ig-mediated blockade of T-cell costimulation in patients with psoriasis vulgaris. J. Clin. Invest. 103, 1243-1252 (1999).
30. Abrams, J. R. et al. Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells. J. Exp. Med. 192, 681-694 (2000).
31. Wolk, K. et al. IL-22 increases the innate immunity of tissues. Immunity 21, 241-254 (2004).
32. Finch, P. W., Murphy, F., Cardinale, I. & Krueger, J. G. Altered expression of keratinocyte growth factor and its receptor in psoriasis. Am. J. Pathol. 151, 1619-1628 (1997).
33. Bowcock, A. M. The genetics of psoriasis and autoimmunity. Annu. Rev. Genomics Hum. Genet. 6, 93-122 (2005).
34. Elder, J. T. et al. The genetics of psoriasis. Arch. Dermatol. 130, 216-224 (1994).
35. Tiilikainen, A., Lassus, A., Karvonen, J., Vartiainen, P. & Julin, M. Psoriasis and HLA-Cw6. Br. J. Dermatol. 102, 179-184 (1980).
36. Veal, C. D. et al. Family-based analysis using a dense single-nucleotide polymorphism-based map defines genetic variation at PSORS1, the major psoriasis-susceptibility locus. Am. J. Hum. Genet. 71, 554-564 (2002).
37. Nair, R. P. et al. Sequence and haplotype analysis supports HLA-C as the psoriasis susceptibility 1 gene. Am. J. Hum. Genet. 78, 827-851 (2006).
38. Helms, C. et al. Localization of PSORS1 to a haplotype block harboring HLA-C and distinct from corneodesmosin and HCR. Hum. Genet. 118, 466-476 (2005).
39. Helms, C. et al. A putative RUNX1 binding site variant between SLC9A3R1 and NAT9 is associated with susceptibility to psoriasis. Nature Genet. 35, 349-356 (2003).
40. Huffmeier, U. et al. Evidence for susceptibility determinant(s) to psoriasis vulgaris in or near PTPN22 in German patients. J. Med. Genet. 43, 517-522 (2006).
41. Tsunemi, Y. et al. Interleukin-12 p40 gene (IL12B) 3′-untranslated region polymorphism is associated with susceptibility to atopic dermatitis and psoriasis vulgaris. J. Dermatol. Sci. 30, 161-166 (2002).
42. Koks, S. et al. Combined haplotype analysis of the interleukin-19 and -20 genes: relationship to plaque-type psoriasis. Genes Immun. 5, 662-667 (2004).
43. Foerster, J. et al. Evaluation of the IRF-2 gene as a candidate for PSORS3. J. Invest. Dermatol. 122, 61-64 (2004).
44. Tomfohrde, J. et al. Gene for familial psoriasis susceptibility mapped to the distal end of human chromosome 17q. Science 264, 1141-1145 (1994).
45. Hwu, W. L. et al. Mapping of psoriasis to 17q terminus. J. Med. Genet. 42, 152-158 (2005).
46. Birnbaum, R. Y. et al. Seborrhea-like dermatitis with psoriasiform elements caused by a mutation in ZNF750, encoding a putative C2H2 zinc finger protein. Nature Genet. 38, 749-751 (2006).
47. Nestle, F. O. & Nickoloff, B. J. From classical mouse models of psoriasis to a spontaneous xenograft model featuring use of AGR mice. Ernst Schering Res. Found. Workshop 203-212 (2005).
48. Villadsen, L. S. et al. Resolution of psoriasis upon blockade of IL-15 biological activity in a xenograft mouse model. J. Clin. Invest. 112, 1571-1580 (2003).
49. Weinberg, J. M., Bottino, C. J., Lindholm, J. & Buchholz, R. Biologic therapy for psoriasis: an update on the tumor necrosis factor inhibitors infliximab, etanercept, and adalimumab, and the T-cell-targeted therapies efalizumab and alefacept. J. Drugs Dermatol. 4, 544-555 (2005).
50. Gottlieb, A. B. Psoriasis: emerging therapeutic strategies. Nature Rev. Drug Discov. 4, 19-34 (2005).
51. Papp, K. A. The long-term efficacy and safety of new biological therapies for psoriasis. Arch. Dermatol. Res. 298, 7-15 (2006).
52. Ellis, C. N. & Krueger, G. G. Treatment of chronic plaque psoriasis by selective targeting of memory effector T lymphocytes. N. Engl. J. Med. 345, 248-255 (2001).
53. Chamian, F. et al. Alefacept reduces infiltrating T cells, activated dendritic cells, and inflammatory genes in psoriasis vulgaris. Proc. Natl Acad. Sci. USA 102, 2075-2080 (2005).
54. + T cells into the skin. Clin. Immunol. 113, 38-46 (2004).
55. Gottlieb, A. B. et al. TNF inhibition rapidly down-regulates multiple proinflammatory pathways in psoriasis plaques. J. Immunol. 175, 2721-2729 (2005).
56. Kruger-Krasagakis, S., Galanopoulos, V. K., Giannikaki, L., Stefanidou, M. & Tosca, A. D. Programmed cell death of keratinocytes in infliximab-treated plaque-type psoriasis. Br. J. Dermatol. 154, 460-466 (2006).
57. Boruchov, A. M. et al. Activating and inhibitory IgG Fc receptors on human DCs mediate opposing functions. J. Clin. Invest. 115, 2914-2923 (2005).
58. Dupasquier, M., Stoitzner, P., van Oudenaren, A., Romani, N. & Leenen, P. J. Macrophages and dendritic cells constitute a major subpopulation of cells in the mouse dermis. J. Invest. Dermatol. 123, 876-879 (2004).
59. Chen, D. M., Gordon, K., Leonardi, C. & Menter, M. A. Adalimumab efficacy and safety in patients with moderate to severe chronic plaque psoriasis: preliminary findings from a 12-week dose-ranging trial. J. Am. Acad. Dermatol. 50, 1 (2004).
60. Gottlieb, A. B. et al. Oral pimecrolimus in the treatment of moderate to severe chronic plaque-type psoriasis: a double-blind, multicentre, randomized, dose-finding trial. Br. J. Dermatol. 152, 1219-1227 (2005).
61. Toichi, E. et al. An anti-IL-12p40 antibody down-regulates type 1 cytokines, chemokines, and IL-12/IL-23 in psoriasis. J. Immunol. 177, 4917-4926 (2006).
62. Xia, Y. P. et al. Transgenic delivery of VEGF to mouse skin leads to an inflammatory condition resembling human psoriasis. Blood 102, 161-168 (2003).
63. Blumberg, H. et al. Interleukin 20: discovery, receptor identification, and role in epidermal function. Cell 104, 9-19 (2001).
64. Zenz, R. et al. Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins. Nature 437, 369-375 (2005).
65. Haider, A. S., Duculan, J., Whynot, J. A. & Krueger, J. G. Increased JunB mRNA and protein expression in psoriasis vulgaris lesions. J. Invest. Dermatol. 126, 912-914 (2006).
66. H17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis. Nature advance online publication (24 December 2006) doi:10.1038/nature05505.