Clinics in Dermatology
Volume 25, Issue 6 , Pages 568-573 , November 2007

The cytokine and chemokine network in psoriasis

  • Brian J. Nickoloff, MD

      Affiliations

    • Department of Pathology and Skin Disease Research Program, Oncology Institute and Cardinal Bernardin Cancer Center, Loyola University Chicago Medical Center, Maywood, IL 60153, USA
    • Corresponding Author InformationCorresponding author.
    • ,
  • Hong Xin, MD

      Affiliations

    • Department of Pathology and Skin Disease Research Program, Oncology Institute and Cardinal Bernardin Cancer Center, Loyola University Chicago Medical Center, Maywood, IL 60153, USA
    • ,
  • Frank O. Nestle, MD

      Affiliations

    • Division of Genetics and Molecular Medicine, King's College London School of Medicine, London SE1 9RT, UK
    • ,
  • Jian-Zhong Qin, MD

      Affiliations

    • Department of Pathology and Skin Disease Research Program, Oncology Institute and Cardinal Bernardin Cancer Center, Loyola University Chicago Medical Center, Maywood, IL 60153, USA

References 

  1. Stern RS, Nijsten T, Feldman SR, Margolis DJ, Rolstad T. Psoriasis is common, carries a substantial burden even when not extensive, and is associated with widespread treatment dissatisfaction. J Investig Dermatol Symp Proc. 2004;9:136–139
  2. Langley RG, Krueger GG, Griffiths CE. Psoriasis: epidemiology, clinical features, and quality of life. Ann Rheum Dis. 2005;64(Suppl 2):ii18–ii23
  3. Hamminga EA, van der Lely AJ, Neumann HA, Thio HB. Chronic inflammation in psoriasis and obesity: implications for therapy. Med Hypotheses. 2006;67:768–773
  4. Neimann AL, Shin DB, Wang X, Margolis DJ, Troxel AB, Gelfand JM. Prevalence of cardiovascular risk factors in patients with psoriasis. J Am Acad Dermatol. 2006;1016
  5. Sommer D, Jenisch S, Suchan M, Christophers E, Weichenthal M. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis. Arch Dermatol Res. 2006;298:321–328
  6. Nickoloff BJ, Nestle FO. Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities. J Clin Invest. 2004;113:1664–1675
  7. Lebwohl M. Psoriasis. Lancet. 2003;361:1197–1204
  8. Esche C, Stellato C, Beck LA. Chemokines: key players in innate and adaptive immunity. J Invest Dermatol. 2005;125:615–628
  9. Zlotnik A, Yoshie O. Chemokines: a new classification system and their role in immunity. Immunity. 2000;12:121–127
  10. Gaspari AA. Innate and adaptive immunity and the pathophysiology of psoriasis. J Am Acad Dermatol. 2006;54:S67–S80
  11. Mackay CR. Chemokines: immunology's high impact factors. Nat Immun. 2001;2:95–101
  12. Robert C, Kupper TS. Inflammatory skin diseases, T cells, and immune surveillance. N Engl J Med. 1999;341:1817–1828
  13. Gordon KB, Nickoloff BJ. Adhesion molecules and inflammatory cell migration pathways in the skin. In:  Bos JD editors. Skin immune system: cutaneous immunology and clinical immunodermatology. Amsterdam: CRC Press; 2004;p. 447–455
  14. Ono SJ, Nakamura T, Miyazaki D, Ohbayashi M, Dawson M, Toda M. Chemokines: roles in leukocyte development, trafficking, and effector function. J Allergy Clin Immunol. 2003;111:1185–1199
  15. Nathan C. Points of control in inflammation. Nature. 2002;420:846–852
  16. Krueger JG, Bowcock A. Psoriasis pathophysiology: current concepts of pathogenesis. Ann Rheum Dis. 2005;64(Suppl 2):ii30–ii36
  17. Bowcock AM, Krueger JG. Getting under the skin: the immunogenetics of psoriasis. Nat Rev Immunol. 2005;5:699–711
  18. Nickoloff BJ, Bonish BK, Marble DJ, et al. Lessons learned from psoriatic plaques concerning mechanisms of tissue repair, remodeling, and inflammation. J Invest Dermatol Symp Proc. 2006;11:16–29
  19. Serhan CN, Savill J. Resolution of inflammation: the beginning programs the end. Nat Immun. 2005;6:1191–1197
  20. Bergers M, van de Kerkhof PC, Happle R, Mier PD. Membrane-bound phospholipase C activity in normal and psoriatic epidermis. Acta Derm Venereol. 1990;70:57–59
  21. Fisher GJ, Talwar HS, Baldassare JJ, Henderson PA, Voorhees JJ. Increased phospholipase C–catalyzed hydrolysis of phosphatidylinositol-4,5-bisphosphate and 1,2-sn-diacylglycerol content in psoriatic involved compared to uninvolved and normal epidermis. J Invest Dermatol. 1990;95:428–435
  22. Luster AD. Chemokines—chemotactic cytokines that mediate inflammation. N Engl J Med. 1998;338:436–445
  23. Luger TA, Stadler BM, Katz SI, Oppenheim JJ. Epidermal cell (keratinocyte)–derived thymocyte-activating factor (ETAF). J Immunol. 1981;127:1493–1498
  24. Mosmann TR, Sad S. The expanding universe of T-cell subsets: Th1, Th2 and more. Immunol Today. 1996;17:138–146
  25. Mosmann TR, Coffman RL. TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. Annu Rev Immunol. 1989;7:145–173
  26. Schön MP, Boehncke WH. Psoriasis. N Engl J Med. 2005;352:1899–1912
  27. Nickoloff BJ. The cytokine network in psoriasis. Arch Dermatol. 1991;127:871–884
  28. Nickoloff BJ, Karabin GD, Barker JN, et al. Cellular localization of interleukin-8 and its inducer, tumor necrosis factor–alpha in psoriasis. Am J Pathol. 1991;138:129–140
  29. Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG. The majority of epidermal T cells in psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor–alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients. J Invest Dermatol. 1999;113:752–759
  30. Ferenczi K, Burack L, Pope M, Krueger JG, Austin LM. CD69, HLA-DR and the IL-2R identify persistently activated T cells in psoriasis vulgaris lesional skin: blood and skin comparisons by flow cytometry. J Autoimmun. 2000;14:63–78
  31. Schlaak JF, Buslau M, Jochum W, et al. T cells involved in psoriasis vulgaris belong to the Th1 subset. J Invest Dermatol. 1994;102:145–149
  32. Uyemura K, Yamamura M, Fivenson DF, Modlin RL, Nickoloff BJ. The cytokine network in lesional and lesion-free psoriatic skin is characterized by a T-helper type 1 cell-mediated response. J Invest Dermatol. 1993;101:701–705
  33. Morhenn VB, Pregerson-Rodan K, Mullen RH, et al. Use of recombinant interferon gamma administered intramuscularly for the treatment of psoriasis. Arch Dermatol. 1987;123:1633–1637
  34. Funk J, Langeland T, Schrumpf E, Hanssen LE. Psoriasis induced by interferon-alpha. Br J Dermatol. 1991;125:463–465
  35. Gottlieb AB, Chamian F, Masud S, et al. TNF inhibition rapidly down-regulates multiple proinflammatory pathways in psoriasis plaques. J Immunol. 2005;175:2721–2729
  36. Li HH, Lin YC, Chen PJ, et al. Interleukin-19 upregulates keratinocyte growth factor and is associated with psoriasis. Br J Dermatol. 2005;153:591–595
  37. Piskin G, Sylva-Steenland RM, Bos JD, Teunissen MB. In vitro and in situ expression of IL-23 by keratinocytes in healthy skin and psoriasis lesions: enhanced expression in psoriatic skin. J Immunol. 2006;176:1908–1915
  38. Wei CC, Chen WY, Wang YC, et al. Detection of IL-20 and its receptors on psoriatic skin. Clin Immunol. 2005;117:65–72
  39. Wittmann M, Purwar R, Hartmann C, Gutzmer R, Werfel T. Human keratinocytes respond to interleukin-18: implication for the course of chronic inflammatory skin diseases. J Invest Dermatol. 2005;124:1225–1233
  40. Wolk K, Witte E, Wallace E, et al. IL-22 regulates the expression of genes responsible for antimicrobial defense, cellular differentiation, and mobility in keratinocytes: a potential role in psoriasis. Eur J Immunol. 2006;36:1309–1323
  41. Mueller W, Herrmann B. Cyclosporin A for psoriasis. Engl J Med. 1979;301:555
  42. Ellis CN, Gorsulowsky DC, Hamilton TA, et al. Cyclosporine improves psoriasis in a double-blind study. JAMA. 1986;256:3110–3116
  43. Krueger GG, Bergstresser PR, Lowe NJ, Voorhees JJ, Weinstein GD. Psoriasis. J Am Acad Dermatol. 1984;11:937–947
  44. Burns MK, Ellis CN, Eisen D, et al. Intralesional cyclosporine for psoriasis. Relationship of dose, tissue levels, and efficacy. Arch Dermatol. 1992;128:786–790
  45. Gottlieb AB, Lebwohl M, Shirin S, et al. Anti-CD4 monoclonal antibody treatment of moderate to severe psoriasis vulgaris: results of a pilot, multicenter, multiple-dose, placebo-controlled study. J Am Acad Dermatol. 2000;43:595–604
  46. Abrams JR, Kelley SL, Hayes E, 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. 2000;192:681–694
  47. Krueger JG. The immunologic basis for the treatment of psoriasis with new biologic agents. J Am Acad Dermatol. 2002;46:1–23
  48. Asadullah K, Döcke WD, Ebeling M, et al. Interleukin 10 treatment of psoriasis: clinical results of a phase 2 trial. Arch Dermatol. 1999;135:187–192
  49. Kimball AB, Kawamura T, Tejura K, et al. Clinical and immunologic assessment of patients with psoriasis in a randomized, double-blind, placebo-controlled trial using recombinant human interleukin 10. Arch Dermatol. 2002;138:1341–1346
  50. Ghoreschi K, Thomas P, Breit S, et al. Interleukin-4 therapy of psoriasis induces Th2 responses and improves human autoimmune disease. Nat Med. 2003;9:40–46
  51. Trepicchio WL, Ozawa M, Walters IB, et al. Interleukin-11 therapy selectively downregulates type I cytokine proinflammatory pathways in psoriasis lesions. J Clin Invest. 1999;104:1527–1537
  52. Nash PT, Florin TH. Tumour necrosis factor inhibitors. Med J Aust. 2005;183:205–208
  53. Gordon KB, Bonish BK, Patel T, Leonardi CL, Nickoloff BJ. The tumour necrosis factor–alpha inhibitor adalimumab rapidly reverses the decrease in epidermal Langerhans cell density in psoriatic plaques. Br J Dermatol. 2005;153:945–953
  54. Krüger-Krasagakis S, Galanopoulos VK, Giannikaki L, Stefanidou M, Tosca AD. Programmed cell death of keratinocytes in infliximab-treated plaque-type psoriasis. Br J Dermatol. 2006;154:460–466
  55. Malaviya R, Sun Y, Tan JK, et al. Etanercept induces apoptosis of dermal dendritic cells in psoriatic plaques of responding patients. J Am Acad Dermatol. 2006;55:590–597
  56. Boyman O, Hefti HP, Conrad C, Nickoloff BJ, Suter M, Nestle FO. Spontaneous development of psoriasis in a new animal model shows an essential role for resident T cells and tumor necrosis factor–alpha. J Exp Med. 2004;199:731–736
  57. Nestle FO, Conrad C, Tun-Kyi A, et al. Plasmacytoid predendritic cells initiate psoriasis through interferon–{alpha} production. J Exp Med. 2005;202:135–143
  58. Nestle FO, Gilliet M. Defining upstream elements of psoriasis pathogenesis: an emerging role for interferon alpha. J Invest Dermatol. 2005;125:xiv–xv
  59. Bhushan M, Bleiker TO, Ballsdon AE, et al. Anti–E-selectin is ineffective in the treatment of psoriasis: a randomized trial. Br J Dermatol. 2002;146:824–831
  60. Schön MP, Krahn T, Schön M, et al. Efomycine M, a new specific inhibitor of selectin, impairs leukocyte adhesion and alleviates cutaneous inflammation. Nat Med. 2002;8:366–372
  61. Toichi E, Torres G, McCormick TS, et al. An anti–IL-12p40 antibody down-regulates type 1 cytokines, chemokines, and IL-12/IL-23 in psoriasis. J Immunol. 2006;177:4917–4926
  62. Iwakura Y, Ishigame H. The IL-23/IL-17 axis in inflammation. J Clin Invest. 2006;116:1218–1222
  63. Kolls JK, Linden A. Interleukin-17 family members and inflammation. Immunity. 2004;21:467–476
  64. Chen Y, Thai P, Zhao YH, Ho YS, DeSouza MM, Wu R. Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. J Biol Chem. 2003;278:17036–17043
  65. Albanesi C, Scarponi C, Cavani A, Federici M, Nasorri F, Girolomoni G. Interleukin-17 is produced by both Th1 and Th2 lymphocytes, and modulates interferon-gamma-and interleukin-4–induced activation of human keratinocytes. J Invest Dermatol. 2000;115:81–87
  66. Kanda N, Koike S, Watanabe S. IL-17 suppresses TNF-alpha–induced CCL27 production through induction of COX-2 in human keratinocytes. J Allergy Clin Immunol. 2005;116:1144–1150
  67. Teunissen MB, Koomen CW, de Waal MR, Wierenga EA, Bos JD. Interleukin-17 and interferon-gamma synergize in the enhancement of proinflammatory cytokine production by human keratinocytes. J Invest Dermatol. 1998;111:645–649
  68. Cataisson C, Pearson AJ, Tsien MZ, et al. CXCR2 ligands and G-CSF mediate PKCalpha-induced intraepidermal inflammation. J Clin Invest. 2006;116:2757–2766
  69. Paniagua RT, Sharpe O, Ho PP, et al. Selective tyrosine kinase inhibition by imatinib mesylate for the treatment of autoimmune arthritis. J Clin Invest. 2006;116:2633–2642
  70. Nickoloff BJ. Keratinocytes regain momentum as instigators of cutaneous inflammation. Trends Mol Med. 2006;12:102–106
  71. Stratis A, Pasparakis M, Rupec RA, et al. Pathogenic role for skin macrophages in a mouse model of keratinocyte-induced psoriasis-like skin inflammation. J Clin Invest. 2006;116:2094–2104
  72. Wang H, Peters T, Kess D, et al. Activated macrophages are essential in a murine model for T cell–mediated chronic psoriasiform skin inflammation. J Clin Invest. 2006;116:2105–2114

PII: S0738-081X(07)00155-1

doi: 10.1016/j.clindermatol.2007.08.011

Clinics in Dermatology
Volume 25, Issue 6 , Pages 568-573 , November 2007

Article Tools

* Image Usage & Resolution