Article information
Abstract
This review emphasizes how translation from bench research to clinical knowledge and vice versa has resulted in considerable progress in understanding the immunopathogenesis of psoriasis. First, the journey in understanding the pathogenic mechanisms behind psoriasis is described. The roles of different components of the adaptive and innate immune systems involved in driving the inflammatory response are explained. Discovery of new immune pathways i.e. the IL23/Th17 axis and its subsequent impact on the development of novel biological therapies is highlighted. Identification of potential targets warranting further research for future therapeutic development are also discussed.
Key words:
psoriasis
immunopathogenesis
T cells
adaptive/innate immune response
Resumen
Esta revisión se centra en el notable progreso que ha generado la aplicación de la investigación básica al conocimiento clínico, y viceversa, en la comprensión de la inmunopatogenia de la psoriasis. Se describe la trayectoria en el conocimiento de los mecanismos patogénicos de la psoriasis; se explican los roles de los diferentes componentes de los sistemas inmunológicos, adaptativo e innato, implicados en la respuesta inflamatoria; se destaca el descubrimiento de nuevas vías inmunológicas, como por ejemplo el eje Il23/Th17 y su posterior impacto en el desarrollo de terapias biológicas novedosas y también se discute la identificación de potenciales dianas que justifican una investigación adicional para el desarrollo terapéutico futuro.
Palabras clave:
psoriasis
inmunopatogenia
células T
respuesta inmunológica adaptativa/innata
Full text is only aviable in PDF
References
[1.]
F.O. Nestle, D.H. Kaplan, J. Barker.
Mechanisms of Disease: Psoriasis.
N Engl J Med, 361 (2009), pp. 496-509
[2.]
T. Henseler, E. Christophers.
Disease concomitance in psoriasis.
J Am Acad Dermatol, 32 (1995), pp. 982-986
[3.]
J.M. Gelfand, A.B. Troxel, J.D. Lewis, S.K. Kurd, D.B. Shin, X. Wang, et al.
The risk of mortality in patients with psoriasis: results from a population-based study.
Arch Dermatol, 143 (2007), pp. 1493-1499
[4.]
B.J. Nickoloff, J.Z. Qin, F.O. Nestle.
Immunopathogenesis of psoriasis.
Clin Rev Allergy Immunol, 33 (2007), pp. 45-56
[5.]
A.M. Bowcock, J.G. Krueger.
Getting under the skin: the immunogenetics of psoriasis.
Nat Rev Immunol, 5 (2005), pp. 699-711
[6.]
C.E. Griffiths, J.N. Barker.
Pathogenesis and clinical features of psoriasis.
Lancet, 370 (2007), pp. 263-271
[7.]
M.A. Lowes, A.M. Bowcock, J.G. Krueger.
Pathogenesis and therapy of psoriasis.
Nature, 445 (2007), pp. 866-873
[8.]
H. Zachariae.
Prevalence of joint disease in patients with psoriasis: implications for therapy.
Am J Clin Dermatol, 4 (2003), pp. 441-447
[9.]
R.W. Eyre, G.G. Krueger.
The Koebner response in psoriasis.
Psoriasis, pp. 105-116
[10.]
J.D. Reveille, M.A. Conant, M. Duvic.
Human immunodeficiency virus-associated psoriasis, psoriatic arthritis, and Reiter's syndrome: a disease continuum?.
Arthritis Rheum, 33 (1990), pp. 1574-1578
[11.]
A.F. Stewart, J. Battaglini-Sabetta, L. Millstone.
Hypocalcemia-induced pustular psoriasis of von Zumbusch. New experience with an old syndrome.
Ann Intern Med, 100 (1984), pp. 677-680
[12.]
D.G. Fortune, H.L. Richards, C.J. Main, C.E. Griffiths.
What patients with psoriasis believe about their condition.
J Am Acad Dermatol, 39 (1998), pp. 196-201
[13.]
M.A. Gupta, A.K. Gupta, S. Kirkby, N.J. Schork, S.K. Gorr, C.N. Ellis, et al.
A psychocutaneous profile of psoriasis patients who are stress reactors. A study of 127 patients.
Gen Hosp Psychiatry, 11 (1989), pp. 166-173
[14.]
E.A. Abel, L.M. DiCicco, E.K. Orenberg, J.E. Fraki, E.M. Farber.
Drugs in exacerbation of psoriasis.
J Am Acad Dermatol, 15 (1986), pp. 1007-1022
[15.]
M. Detmar, L.F. Brown, K.P. Claffey, K.T. Yeo, O. Kocher, R.W. Jackman, et al.
Overexpression of vascular permeability factor/ vascular endothelial growth factor and its receptors in psoriasis.
J Exp Med, 180 (1994), pp. 1141-1146
[16.]
J. Holash, P.C. Maisonpierre, D. Compton, P. Boland, C.R. Alexander, D. Zagzag, et al.
Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF.
Science, 284 (1999), pp. 1994-1998
[17.]
K. Kuroda, A. Sapadin, T. Shoji, R. Fleischmajer, M. Lebwohl.
Altered expression of angiopoietins and Tie2 endothelium receptor in psoriasis.
J Invest Dermatol, 116 (2001), pp. 713-720
[18.]
A.L. Neimann, D.B. Shin, X. Wang, D.J. Margolis, A.B. Troxel, J.M. Gelfand.
Prevalence of cardiovascular risk factors in patients with psoriasis.
J Am Acad Dermatol, 55 (2006), pp. 829-835
[19.]
D.M. Sommer, S. Jenisch, M. Suchan, E. Christophers, M. Weichenthal.
Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis.
Arch Dermatol Res, 298 (2006), pp. 321-328
[20.]
J.M. Gelfand, A.L. Neimann, D.B. Shin, X. Wang, D.J. Margolis, A.B. Troxel.
Risk of myocardial infarction in patients with psoriasis.
JAMA, 296 (2006), pp. 1735-1741
[21.]
M. Esposito, R. Saraceno, A. Giunta, M. Maccarone, S. Chimenti.
An Italian study on psoriasis and depression.
Dermatology, 212 (2006), pp. 123-127
[22.]
U. Mrowietz, J.T. Elder, J. Barker.
The importance of disease associations and concomitant therapy for the long-term management of psoriasis patients.
Arch Dermatol Res, 298 (2006), pp. 309-319
[23.]
P. Rahman, J.T. Elder.
Genetic epidemiology of psoriasis and psoriatic arthritis.
Ann Rheum Dis, 64 (2005), pp. ii37-ii39
[24.]
F. Capon, R.C. Trembath, J.N. Barker.
An update on the genetics of psoriasis.
Dermatol Clin, 22 (2004), pp. 339-347
[25.]
A. Morris, M. Rogers, G. Fischer, K. Williams.
Childhood psoriasis: a clinical review of 1262 cases.
Pediatr Dermatol, 18 (2001), pp. 188-198
[26.]
W. Watson, H.M. Cann, E.M. Farber, M.L. Nall.
The genetics of psoriasis.
Arch Dermatol, 105 (1972), pp. 197-207
[27.]
M. Theeuwes, R.O. Leder.
Hereditary insights in psoriasis.
Eur J Dermatol, 3 (1993), pp. 335-341
[28.]
F. Brandrup, M. Hauge, K. Henningsen, B. Eriksen.
Psoriasis in an unselected series of twins.
Arch Dermatol, 114 (1978), pp. 874-878
[29.]
D.L. Duffy, L.S. Spelman, N.G. Martin.
Psoriasis in Australian twins.
J Am Acad Dermatol, 29 (1993), pp. 428-434
[30.]
E.M. Farber, M.L. Nall, W. Watson.
Natural history of psoriasis in 61 twin pairs.
Arch Dermatol, 109 (1974), pp. 207-211
[31.]
M. Pisani, V. Ruocco.
‘Twin’ psoriasis in monozygotic twins.
Arch Dermatol, 120 (1984), pp. 1418-1419
[32.]
R.P. Nair, P.E. Stuart, I. Nistor, R. Hiremagalore, N.V. Chia, S. Jenisch, et al.
Sequence and haplotype analysis supports HLA-C as the psoriasis susceptibility 1 gene.
Am J Hum Genet, 78 (2006), pp. 827-851
[33.]
R.C. Trembath, R.L. Clough, J.L. Rosbotham, A.B. Jones, R.D. Camp, A. Frodsham, et al.
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 (1997), pp. 813-820
[34.]
F. Capon, M.J. Bijlmakers, N. Wolf, M. Quaranta, U. Huffmeier, M. Allen, et al.
Identification of ZNF313/RNF114 as a novel psoriasis susceptibility gene.
Hum Mol Genet, 17 (2008), pp. 1938-1945
[35.]
F. Capon, P. Di Meglio, J. Szaub, N.J. Prescott, C. Dunster, L. Baumber, et al.
Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis.
Hum Genet, 122 (2007), pp. 201-206
[36.]
E. Mallon, R. Newson, C.B. Bunker.
HLA-Cw6 and the genetic predisposition to psoriasis: a meta-analysis of published serologic studies.
J Invest Dermatol, 113 (1999), pp. 693-695
[37.]
J.E. Gudjonsson, A. Karason, A. Antonsdottir, E.H. Runarsdottir, V.B. Hauksson, R. Upmanyu, et al.
Psoriasis patients who are homozygous for the HLA-Cw*0602 allele have a 2.5-fold increased risk of developing psoriasis compared with Cw6 heterozygotes.
Br J Dermatol, 148 (2003), pp. 233-235
[38.]
T. Henseler, E. Christophers.
Psoriasis of early and late onset: characterization of two types of psoriasis vulgaris.
J Am Acad Dermatol, 13 (1985), pp. 450-456
[39.]
J.E. Gudjonsson, A. Karason, E.H. Runarsdottir, A.A. Antonsdottir, V.B. Hauksson, H.H. Jonsson, et al.
Distinct clinical differences between HLA-Cw*0602 positive and negative psoriasis patients-an analysis of 1019 HLA-C- and HLA-B-typed patients.
J Invest Dermatol, 126 (2006), pp. 740-745
[40.]
X. Fan, S. Yang, L.D. Sun, Y.H. Liang, M. Gao, K.Y. Zhang, et al.
Comparison of clinical features of HLA-Cw*0602-positive and -negative psoriasis patients in a Han Chinese population.
Acta Derm Venereol, 87 (2007), pp. 335-340
[41.]
N.R. Telfer, R.J. Chalmers, K. Whale, G. Colman.
The role of streptococcal infection in the initiation of guttate psoriasis.
Arch Dermatol, 128 (1992), pp. 39-42
[42.]
J.C. Prinz.
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 (2001), pp. 326-332
[43.]
B.J. Nickoloff.
Skin innate immune system in psoriasis: friend or foe?.
J Clin Invest, 104 (1999), pp. 1161-1164
[44.]
M.P. Martin, G. Nelson, J.H. Lee, F. Pellett, X. Gao, J. Wade, et al.
Cutting edge: susceptibility to psoriatic arthritis: influence of activating killer Ig-like receptor genes in the absence of specific HLA-C alleles.
J Immunol, 169 (2002), pp. 2818-2822
[45.]
J.G. Krueger.
The immunologic basis for the treatment of psoriasis with new biologic agents.
J Am Acad Dermatol, 46 (2002), pp. 1-23
[46.]
B.S. McKenzie, R.A. Kastelein, D.J. Cua.
Understanding the IL-23-IL-17 immune pathway.
Trends Immunol, 27 (2006), pp. 17-23
[47.]
H. Sugiyama, R. Gyulai, E. Toichi, E. Garaczi, S. Shimada, S.R. Stevens, et al.
Dysfunctional blood and target tissue CD4+ CD25 high regulatory T cells in psoriasis: mechanism underlying unrestrained pathogenic effector T cell proliferation.
J Immunol, 174 (2005), pp. 164-173
[48.]
A.A. Gaspari.
Innate and adaptive immunity and the pathophysiology of psoriasis.
J Am Acad Dermatol, 54 (2006), pp. S67-S80
[49.]
K. Ghoreschi, P. Thomas, S. Breit, M. Dugas, R. Mailhammer, W. van Eden, et al.
Interleukin-4 therapy of psoriasis induces Th2 responses and improves human autoimmune disease.
Nat Med, 9 (2003), pp. 40-46
[50.]
K. Asadullah, W.D. Docke, M. Ebeling, M. Friedrich, G. Belbe, H. Audring, et al.
Interleukin 10 treatment of psoriasis: clinical results of a phase 2 trial.
Arch Dermatol, 135 (1999), pp. 187-192
[51.]
W. Lew, A.M. Bowcock, J.G. Krueger.
Psoriasis vulgaris: cutaneous lymphoid tissue supports T-cell activation and “Type 1” inflammatory gene expression.
Trends Immunol, 25 (2004), pp. 295-305
[52.]
C.L. Leonardi, J.L. Powers, R.T. Matheson, B.S. Goffe, R. Zitnik, A. Wang, et al.
Etanercept as monotherapy in patients with psoriasis.
N Engl J Med, 349 (2003), pp. 2014-2022
[53.]
U. Chaudhari, P. Romano, L.D. Mulcahy, L.T. Dooley, D.G. Baker, A.B. Gottlieb.
Efficacy and safety of infliximab monotherapy for plaque-type psoriasis: a randomised trial.
Lancet, 357 (2001), pp. 1842-1847
[54.]
T. Patel, K.B. Gordon.
Adalimumab: efficacy and safety in psoriasis and rheumatoid arthritis.
Dermatol Ther, 17 (2004), pp. 427-431
[55.]
B.B. Simen, C.H. Duman, A.A. Simen, R.S. Duman.
TNFalpha signaling in depression and anxiety: behavioral consequences of individual receptor targeting.
Biol Psychiatry, 59 (2006), pp. 775-785
[56.]
S. Tyring, A. Gottlieb, K. Papp, K. Gordon, C. Leonardi, A. Wang, et al.
Etanercept and clinical outcomes, fatigue, and depression in psoriasis: double-blind placebo-controlled randomised phase III trial.
Lancet, 367 (2006), pp. 29-35
[57.]
G.G. Krueger, P.R. Bergstresser, N.J. Lowe, J.J. Voorhees, G.D. Weinstein.
Psoriasis.
J Am Acad Dermatol, 11 (1984), pp. 937-947
[58.]
C.N. Ellis, D.C. Gorsulowsky, T.A. Hamilton, J.K. Billings, M.D. Brown, J.T. Headington, et al.
Cyclosporine improves psoriasis in a double-blind study.
JAMA, 256 (1986), pp. 3110-3116
[59.]
B.S. Baker, C.E. Griffiths, S. Lambert, A.V. Powles, J.N. Leonard, H. Valdimarsson, et al.
The effects of cyclosporin A on T lymphocyte and dendritic cell sub-populations in psoriasis.
Br J Dermatol, 116 (1987), pp. 503-510
[60.]
B.V. Jegasothy, C.D. Ackerman, S. Todo, J.J. Fung, K. Abu-Elmagd, T.E. Starzl.
Tacrolimus (FK 506)–a new therapeutic agent for severe recalcitrant psoriasis.
Arch Dermatol, 128 (1992), pp. 781-785
[61.]
J. Prinz, O. Braun-Falco, M. Meurer, P. Daddona, C. Reiter, P. Rieber, et al.
Chimaeric CD4 monoclonal antibody in treatment of generalised pustular psoriasis.
Lancet, 338 (1991), pp. 320-321
[62.]
S.L. Gottlieb, P. Gilleaudeau, R. Johnson, L. Estes, T.G. Woodworth, A.B. Gottlieb, et al.
Response of psoriasis to a lymphocyte-selective toxin (DAB389IL-2) suggests a primary immune, but not keratinocyte, pathogenic basis.
Nat Med, 1 (1995), pp. 442-447
[63.]
J.R. Abrams, M.G. Lebwohl, C.A. Guzzo, B.V. Jegasothy, M.T. Goldfarb, B.S. Goffe, et al.
CTLA4Ig-mediated blockade of T-cell costimulation in patients with psoriasis vulgaris.
J Clin Invest, 103 (1999), pp. 1243-1252
[64.]
J.R. Abrams, S.L. Kelley, E. Hayes, T. Kikuchi, M.J. Brown, S. Kang, 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 (2000), pp. 681-694
[65.]
A. Menssen, P. Trommler, S. Vollmer, D. Schendel, E. Albert, L. Gurtler, et al.
Evidence for an antigen-specific cellular immune response in skin lesions of patients with psoriasis vulgaris.
J Immunol, 155 (1995), pp. 4078-4083
[66.]
C. Conrad, O. Boyman, G. Tonel, A. Tun-Kyi, U. Laggner, A. de Fougerolles, et al.
Alpha1beta1 integrin is crucial for accumulation of epidermal T cells and the development of psoriasis.
Nat Med, 13 (2007), pp. 836-842
[67.]
A. Di Cesare, P. Di Meglio, F.O. Nestle.
The IL-23/Th17 Axis in the Immunopathogenesis of Psoriasis.
J Invest Dermatol, 129 (2009), pp. 1339-1350
[68.]
B. Oppmann, R. Lesley, B. Blom, J.C. Timans, Y. Xu, B. Hunte, et al.
Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12.
Immunity, 13 (2000), pp. 715-725
[69.]
J.R. Chan, W. Blumenschein, E. Murphy, C. Diveu, M. Wiekowski, S. Abbondanzo, et al.
IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis.
J Exp Med, 203 (2006), pp. 2577-2587
[70.]
Y. Zheng, D.M. Danilenko, P. Valdez, I. Kasman, J. Eastham-Anderson, J. Wu, et al.
Interleukin-22, a T(H)17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis.
Nature, 445 (2007), pp. 648-651
[71.]
G. Piskin, R.M. Sylva-Steenland, J.D. Bos, M.B. Teunissen.
In vitro and in situ expression of IL-23 by keratinocytes in healthy skin and psoriasis lesions: enhanced expression in psoriatic skin.
J Immunol, 176 (2006), pp. 1908-1915
[72.]
G. Piskin, U. Tursen, R.M. Sylva-Steenland, J.D. Bos, M.B. Teunissen.
Clinical improvement in chronic plaque-type psoriasis lesions after narrow-band UVB therapy is accompanied by a decrease in the expression of IFN-gamma inducers –IL-12, IL-18 and IL-23.
Exp Dermatol, 13 (2004), pp. 764-772
[73.]
A.B. Gottlieb, F. Chamian, S. Masud, I. Cardinale, M.V. Abello, M.A. Lowes, et al.
TNF inhibition rapidly down-regulates multiple proinflammatory pathways in psoriasis plaques.
J Immunol, 175 (2005), pp. 2721-2729
[74.]
A.S. Haider, M.A. Lowes, M. Suárez-Farinas, L.C. Zaba, I. Cardinale, A. Khatcherian, 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, 180 (2008), pp. 1913-1920
[75.]
C.L. Langrish, Y. Chen, W.M. Blumenschein, J. Mattson, B. Basham, J.D. Sedgwick, et al.
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation.
J Exp Med, 201 (2005), pp. 233-240
[76.]
C.L. Kauffman, N. Aria, E. Toichi, T.S. McCormick, K.D. Cooper, A.B. Gottlieb, et al.
A phase I study evaluating the safety, pharmacokinetics, and clinical response of a human IL-12 p40 antibody in subjects with plaque psoriasis.
J Invest Dermatol, 123 (2004), pp. 1037-1044
[77.]
G.G. Krueger, R.G. Langley, C. Leonardi, N. Yeilding, C. Guzzo, Y. Wang, et al.
A human interleukin-12/23 monoclonal antibody for the treatment of psoriasis.
N Engl J Med, 356 (2007), pp. 580-592
[78.]
A.B. Kimball, K.B. Gordon, R.G. Langley, A. Menter, E.K. Chartash, J. Valdes.
Safety and efficacy of ABT-874, a fully human interleukin 12/23 monoclonal antibody, in the treatment of moderate to severe chronic plaque psoriasis: results of a randomized, placebo-controlled, phase 2 trial.
Arch Dermatol, 144 (2008), pp. 200-207
[79.]
C.L. Leonardi, A.B. Kimball, K.A. Papp, N. Yeilding, C. Guzzo, Y. Wang, et al.
Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 76-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 1).
Lancet, 371 (2008), pp. 1665-1674
[80.]
K.A. Papp, R.G. Langley, M. Lebwohl, G.G. Krueger, P. Szapary, N. Yeilding, et al.
Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 52-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 2).
Lancet, 371 (2008), pp. 1675-1684
[81.]
A. Gottlieb, A. Menter, A. Mendelsohn, Y.K. Shen, S. Li, C. Guzzo, et al.
Ustekinumab, a human interleukin 12/23 monoclonal antibody, for psoriatic arthritis: randomised, double-blind, placebo-controlled, crossover trial.
Lancet, 373 (2009), pp. 633-640
[82.]
D.C. Gondek, L.F. Lu, S.A. Quezada, S. Sakaguchi, R.J. Noelle.
Cutting edge: contact-mediated suppression by CD4+CD25+ regulatory cells involves a granzyme B-dependent, perforin- independent mechanism.
J Immunol, 174 (2005), pp. 1783-1786
[83.]
O. Annacker, C. Asseman, S. Read, F. Powrie.
Interleukin- 10 in the regulation of T cell-induced colitis.
J Autoimmun, 20 (2003), pp. 277-279
[84.]
K. Nakamura, A. Kitani, I. Fuss, A. Pedersen, N. Harada, H. Nawata, et al.
TGF-beta 1 plays an important role in the mechanism of CD4+CD25+ regulatory T cell activity in both humans and mice.
J Immunol, 172 (2004), pp. 834-842
[85.]
O. Baadsgaard, B. Salvo, A. Mannie, B. Dass, D.A. Fox, K.D. Cooper.
In vivo ultraviolet-exposed human epidermal cells activate T suppressor cell pathways that involve CD4+CD45RA+ suppressor-inducer T cells.
J Immunol, 145 (1990), pp. 2854-2861
[86.]
Nestle FO, Nickoloff BJ. From classical mouse models of psoriasis to a spontaneous xenograft model featuring use of AGR mice. Ernst Schering Res Found Workshop; 2005. p. 203-12.
[87.]
M.P. Schon.
Animal models of psoriasis: a critical appraisal.
Exp Dermatol, 17 (2008), pp. 703-712
[88.]
J.E. Gudjonsson, A. Johnston, M. Dyson, H. Valdimarsson, J.T. Elder.
Mouse models of psoriasis.
J Invest Dermatol, 127 (2007), pp. 1292-1308
[89.]
O. Boyman, H.P. Hefti, C. Conrad, B.J. Nickoloff, M. Suter, F.O. Nestle.
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, 199 (2004), pp. 731-736
[90.]
F.O. Nestle, C. Conrad, A. Tun-Kyi, B. Homey, M. Gombert, O. Boyman, et al.
Plasmacytoid predendritic cells initiate psoriasis through interferon-alpha production.
J Exp Med, 202 (2005), pp. 135-143
[91.]
P. Schmid, P. Itin, D. Cox, G.K. McMaster, M.A. Horisberger.
The type I interferon system is locally activated in psoriatic lesions.
J Interferon Res, 14 (1994), pp. 229-234
[92.]
L. van der Fits, L.I. van der Wel, J.D. Laman, E.P. Prens, M.C. Verschuren.
In psoriasis lesional skin the type I interferon signaling pathway is activated, whereas interferon-alpha sensitivity is unaltered.
J Invest Dermatol, 122 (2004), pp. 51-60
[93.]
M. Gilliet, C. Conrad, M. Geiges, A. Cozzio, W. Thurlimann, G. Burg, et al.
Psoriasis triggered by toll-like receptor 7 agonist imiquimod in the presence of dermal plasmacytoid dendritic cell precursors.
Arch Dermatol, 140 (2004), pp. 1490-1495
[94.]
A.N. Theofilopoulos, R. Baccala, B. Beutler, D.H. Kono.
Type I interferons (alpha/beta) in immunity and autoimmunity.
Annu Rev Immunol, 23 (2005), pp. 307-336
[96.]
B.S. Baker, J.D. Laman, A. Powles, L. van der Fits, J.S. Voerman, M.J. Melief, et al.
Peptidoglycan and peptidoglycan-specific Th1 cells in psoriatic skin lesions.
J Pathol, 209 (2006), pp. 174-181
[97.]
A. Johnston, J.E. Gudjonsson, H. Sigmundsdottir, T.J. Love, H. Valdimarsson.
Peripheral blood T cell responses to keratin peptides that share sequences with streptococcal M proteins are largely restricted to skin-homing CD8(+) T cells.
Clin Exp Immunol, 138 (2004), pp. 83-93
[98.]
J.P. McFadden, B.S. Baker, A.V. Powles, L. Fry.
Psoriasis and streptococci: the natural selection of psoriasis revisited.
Br J Dermatol, 160 (2009), pp. 929-937
[99.]
E.K. Pias, J. Hilario-Vargas, N. Li, L.A. Diaz.
Humoral autoimmunity in pemphigus.
Autoimmunity, 37 (2004), pp. 283-286
[100.]
R. Lande, J. Gregorio, V. Facchinetti, B. Chatterjee, Y.H. Wang, B. Homey, et al.
Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide.
Nature, 449 (2007), pp. 564-569
Copyright © 2009. Academia Española de Dermatología y Venereología
