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References
Gottlieb A. Psoriasis. Dis Manag Clin Outcome. 1998;1:195–202.
Gaspari AA. Innate and adaptive immunity and the pathophysiology of psoriasis. J Am Acad Dermatol. 2006;54(3 suppl 2):S67–80.
Di Cesare A, Di Meglio P, Nestle F. The IL-23/Th17 axis in the immunopathogenesis of psoriasis. J Invest Dermatol. 2009;129:1339–50.
Barker J. The pathophysiology of psoriasis. Lancet. 1991;338:227–30.
Nickoloff BJ, Nestle FO. Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities. J Clin Invest. 2004;113:1664–75.
Bos J, Meinardi M, van Joost T, et al. Use of cyclosporine in psoriasis. Lancet. 1989;23:1500–5.
Khandke L, Krane J, Ashinoff R, et al. Cyclosporine in psoriasis treatment: inhibition of keratinocyte cell-cycle progression in G1 independent effects on transforming growth factor-alpha/epidermal growth factor receptor pathways. Arch Dermatol. 1991;127:1172–9.
Gottlieb S, Gilleaudeau P, Johnson R, et al. Response of psoriasis to a lymphocyte-selective toxin (DAB389IL-2) suggests a primary immune, but not keratinocyte, pathogenic basis. Nat Med. 1995;1:442–7.
Vallat V, Gilleaudeau P, Battat L, et al. PUVA bath therapy strongly suppresses immunological and epidermal activation in psoriasis: a possible cellular basis for remittive therapy. J Exp Med. 1994;180:283–96.
Gottlieb A, Grossman R, Khandke L, et al. Studies of the effect of cyclosporine in psoriasis in vivo: combined effects on activated T lymphocytes and epidermal regenerative maturation. J Invest Dermatol. 1992;98:302–9.
Gottlieb S, Hayes E, Gilleaudeau P, et al. Cellular actions of etretinate in psoriasis: enhanced epidermal differentiation and reduced cell-mediated inflammation are unexpected outcomes. J Cutan Pathol. 1996;23:404–18.
Nickoloff B, Bonish B, Huang B, et al. Characterization of a T cell line bearing natural killer receptors and capable of creating psoriasis in a SCID mouse model system. J Dermatol Sci. 2000;24:212–25.
Gillet M, Conrad C, Geiges M, et al. Psoriasis triggered by toll-like receptor 7 agonist imiquimod in the presence of dermal plasmacytoid dendritic cell precursors. Arch Dermatol. 2004;140:1490–5.
Funk J, Langeland T, Schrumpf E, et al. Psoriasis induced by interferon-alpha. Br J Dermatol. 1991;125:463–5.
Shiohara T, Kobayahsi M, Abe K, et al. Psoriasis occurring predominantly on warts: possible involvement of interferon alpha. Arch Dermatol. 1988;124:1816–21.
Fierlbeck G, Rassner G, Muller C. Psoriasis induced at the injection site of recombinant interferon gamma: results of immunohistologic investigations. Arch Dermatol. 1990;126:351–5.
Prinz J. The role of T cells in psoriasis. J Eur Acad Dermatol Venereol. 2003;17(suppl):1–5.
Bos J, de Rie M. The pathogenesis of psoriasis: immunological facts and speculations. Immunol Today. 1999;20:40–6.
Geginat J, Campagnaro S, Sallusto F, et al. TCR-independent proliferation and differentiation of human CD4+ T cell subsets induced by cytokines. Adv Exp Med Biol. 2002;512:107–12.
Kastelan M, Massari L, Brajac I. Apoptosis mediated by cytolytic molecules might be responsible for maintenance of psoriatic plaques. Med Hypotheses. 2006;67:336–7.
Austin L, Ozawa M, Kikuchi T, et al. 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;113:752–9.
Abrams J, Kelley S, Hayes E, et al. Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plagues, including the activation of keratinocytes, dendritic cells and endothelial cells. J Exp Med. 2000;192:681–94.
Lebwohl M, Christophers E, Langley R, et al. An international, randomized, double-blind, placebo-controlled phase 3 trial of intramuscular alefacept in patients with chronic plaque psoriasis. Arch Dermatol. 2003;139:719–27.
Krueger G, Ellis C. Alefacept therapy produces remission for patients with chronic plaque psoriasis. Br J Dermatol. 2003;148:784–8.
Gordon K, Leonardi C, Tyring S, et al. Efalizumab (anti-CD11a) is safe and effective in the treatment of psoriasis: pooled results of the 12-week first treatment period from 2 phase III trials. J Invest Dermatol. 2002;119:242.
Singh A, Wilson M, Hong S, et al. Natural killer T cell activation protects mice against experimental autoimmune encephalomyelitis. J Exp Med. 2001;194:1801–11.
Saubermann L, Beck P, De Jong Y, et al. Activation of natural killer T cells by alpha-glactosylceramide in the presence of CD1d provides protection against colitis in mice. Gastroenterology. 2000;119:119–28.
Campos R, Szczepanik M, Itakura A, et al. Cutaneous immunization rapidly activates liver invariant Valpha 14 NKT cells stimulating B-1 B cells to initiate T cell recruitment for elicitation of contact sensitivity. J Exp Med. 2003;198:1785–96.
Bonish B, Jullien D, Dutronc Y, et al. Overexpression of CD1d by keratinocytes in psoriasis and CD1d-dependent IFN-gamma production by NK-T cells. J Immunol. 2000;165:4076–85.
Deguchi M, Aiba S, Ohtani H, et al. Comparison of the distribution and numbers of antigen-presenting cells among T-lymphocyte-mediated dermatoses: CD1a+, factor XIIIa+, and CD68+ cells in eczematous dermatitis, psoriasis, lichen planus and graft-versus-host disease. Arch Dermatol Res. 2002;294:297–302.
Bos J, de Rie M, Teunissen M, et al. Psoriasis: dysregulation of innate immunity. Br J Dermatol. 2005;152:1098–107.
Trefzer U, Hofmann M, Sterry W, et al. Cytokine and anticytokine therapy in dermatology. Expert Opin Biol Ther. 2003;3:733–43.
Nickoloff B. The cytokine network in psoriasis. Arch Dermatol. 1991;127:871–84.
Victor F, Gottlieb A. TNF-alpha and apoptosis: implications for the pathogenesis and treatment of psoriasis. J Drugs Dermatol. 2002;3:264–75.
Oh C, Das K, Gottlieb A. Treatment with anti-tumour necrosis factor alpha (TNF-alpha) monoclonal antibody dramatically decreases the clinical activity of psoriasis lesions. J Am Acad Dermatol. 2000;42:829–30.
Reich K, Nestle FO, Papp K, EXPRESS study investigators, et al. Infliximab induction and maintenance therapy for moderate-to-severe psoriasis: a phase III, multicentre, double-blind trial. Lancet. 2005;366:1367–74.
Leonardi C, Powers J, Matheson R, et al. Etanercept as monotherapy in patients with psoriasis. N Engl J Med. 2003;349:2014–22.
Saini R, Tutrone W, Weinberg J. Advances in therapy for psoriasis: an overview of infliximab, etanercept, efalizumab, alefacept, adalimumab, tazarotene, and pimecrolimus. Curr Pharm Des. 2005;11:273–80.
Cosmi L, De Palma R, Santarlasci V, et al. Human interleukin 17-producing cells originate from a CD161+CD4+ T cell precursor. J Exp Med. 2008;205:1903–16.
de Beaucoudrey L, Puel A, Filipe-Santos O, et al. Mutations in STAT3 and IL12RB1 impair the development of human IL-17-producing T cells. J Exp Med. 2008;205:1543–50.
Manel N, Unutmaz D, Littman DR. The differentiation of human T(H)-17 cells requires transforming growth factor-beta and induction of the nuclear receptor RORgammat. Nat Immunol. 2008;9:641–9.
Yang L, Anderson DE, Baecher-Allan C, et al. IL-21 and TGF-beta are required for differentiation of human T(H)17 cells. Nature. 2008;454:350–2.
Lee E, Trepicchio WL, Oestreicher JL, et al. Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris. J Exp Med. 2004;199:125–30.
Chan JR, Blumenschein W, Murphy E, et al. IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis. J Exp Med. 2006;203:2557–87.
Capon F, Di Meglio P, Szaub J, et al. Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis. Hum Genet. 2007;122:201–6.
Cargill M, Schrodi SJ, Chang M, et al. A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes. Am J Hum Genet. 2007;80:273–90.
Nair RP, Ruether A, Stuart PE, et al. Polymorphisms of the IL12B and IL23R genes are associated with psoriasis. J Invest Dermatol. 2008;128:1653–61.
Ma HL, Liang S, Li J, et al. IL-22 is required for Th17 cell-mediated pathology in a mouse model of psoriasis-like skin inflammation. J Clin Invest. 2008;118:597–607.
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;36:1309–23.
Boniface K, Guignouard E, Pedretti N, et al. A role for T cell-derived interleukin 22 in psoriatic skin inflammation. Clin Exp Immunol. 2007;150:407–15.
Weaver CT, Hatton RD, Mangan PR, et al. IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu Rev Immunol. 2007;25:821–52.
Teunissen MB, Koomen CW, de Waal MR, et al. Interleukin-17 and interferon-gamma synergize in the enhancement of proinflammatory cytokine production by human keratinocytes. J Invest Dermatol. 1998;111:645–9.
Lowes MA, Kikuchi T, Fuentes-Duculan J, et al. Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells. J Invest Dermatol. 2008;128:1207–11.
Arican O, Aral M, Sasmaz S, et al. Serum levels of TNF-alpha, IFN-gamma, IL-6, IL-8, IL-12, IL-17, and IL-18 in patients with active psoriasis and correlation with disease severity. Mediat Inflamm. 2005;2005:273–9.
Zaba LC, Cardinale I, Gilleaudeau P, et al. Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses. J Exp Med. 2007;204:3183–94.
Haider AS, Cohen J, Fei J, et al. Insights into gene modulation by therapeutic TNF and IFNgamma antibodies: TNF regulates IFNgamma production by T cells and TNF-regulated genes linked to psoriasis transcriptome. J Invest Dermatol. 2008;128:655–66.
Haider AS, Lowes MA, Suarez-Farinas M, et al. Identification of cellular pathways of “type 1,” Th17 T cells, and TNF- and inducible nitric oxide synthase-producing dendritic cells in autoimmune inflammation through pharmacogenomic study of cyclosporine a in psoriasis. J Immunol. 2008;180:1913–20.
Croxtall JD. Ustekinumab: a review of its use in the management of moderate to severe plaque psoriasis. Drugs. 2011;71:1733–53.
Gordon KB, Langely RG, Gottlieb AB, et al. A phase III, randomized, controlled trial of the fully human IL-12/23 mAb briakinumab in moderate-to-severe psoriasis. J Invest Dermatol. 2012;132:304–14.
Rahman P, Elder JT. Genetic epidemiology of psoriasis and psoriatic arthritis. Ann Rheum Dis. 2005;64(suppl 2):ii37–9.
Elder JT. PSORS1: linking genetics and immunology. J Invest Dermatol. 2006;126:1205–6.
Krueger JG, Bowcock A. Psoriasis pathophysiology: current concepts of pathogenesis. Ann Rheum Dis. 2005;64(suppl 2):ii30–6.
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Hugh, J.M., Weinberg, J.M. (2021). Pathophysiology of Psoriasis/Novel Pathways. In: Weinberg, J.M., Lebwohl, M. (eds) Advances in Psoriasis. Springer, Cham. https://doi.org/10.1007/978-3-030-54859-9_2
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