Indian Journal of Dermatology
  Publication of IADVL, WB
  Official organ of AADV
Indexed with Science Citation Index (E) , Web of Science and PubMed
Users online: 1041  
Home About  Editorial Board  Current Issue Archives Online Early Coming Soon Guidelines Subscriptions  e-Alerts    Login  
    Small font sizeDefault font sizeIncrease font size Print this page Email this page

Year : 2009  |  Volume : 54  |  Issue : 1  |  Page : 7-12
Current concepts in the pathogenesis of psoriasis

1 Institute of Pathology (ICMR), Safdarjang Hospital and Vardhman Mahavir Medical College, New Delhi, India
2 Department of Dermatology and Regional STD Centre, Safdarjang Hospital and Vardhman Mahavir Medical College, New Delhi, India

Correspondence Address:
Arun Kumar Jain
Institute of Pathology (ICMR), PB#4909, Safdarjang Hospital Campus, New Delhi - 110 029
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-5154.48977

Clinical trial registration None

Rights and Permissions


Psoriasis is a multi-factorial skin disease with a complex pathogenesis. Various factors which have been suggested to play a key role in the pathogenesis are T cells, antigen presenting cells (APC's), keratinocytes, Langerhans' cells, macrophages, natural killer cells, an array of Th1 type cytokines, certain growth factors like vascular endothelial growth factor (VEGF), keratinocyte growth factor (KGF), and others. It has been hypothesized that the disease starts with the activation of T cell by an unknown antigen, which leads to secretion of an array of cytokines by activated T cells, inflammatory cells, and keratinocytes. The characteristic lesion of psoriasis is due to the hyper-proliferation of the keratinocyte. Activated Langerhans' cells migrate from skin to lymph nodes presenting the antigen to nodal naοve T cells (cells that have not been activated by antigen previously). The T cells activated by non-antigen-dependent mechanism may, however, become antigen-specific memory cells that react with a cross-reactive auto-antigen such as keratin (molecular mimicry). The genetic background of the disease may be suggested from the fact that concordance rate is 63-73% in monozygotic twins, as compared to 17-20% in dizygotic twins. Several disease susceptibility loci have been suggested as predisposing factors, PSORS1-PSORS9.

Keywords: Autoimmunity, pathogenesis, psoriasis

How to cite this article:
Das RP, Jain AK, Ramesh V. Current concepts in the pathogenesis of psoriasis. Indian J Dermatol 2009;54:7-12

How to cite this URL:
Das RP, Jain AK, Ramesh V. Current concepts in the pathogenesis of psoriasis. Indian J Dermatol [serial online] 2009 [cited 2022 Sep 25];54:7-12. Available from:

   Introduction Top

Whether psoriasis represents a fundamental disease of skin, or the immune system, has been debated for several years. Role of T cells, antigen-presenting cells, keratinocytes, Langerhans' cell, macrophages, natural killer cells, an array of Th1 type cytokines, certain growth factors like vascular endothelial growth factor (VEGF) keratinocyte growth factor (KGF) and others have been suggested to play a key role in pathogenesis of psoriasis. Currently a wide array of treatment modalities is available for psoriasis, but with every treatment there is a possibility of remission. Systemic or UV photo-therapies may have unacceptable side effects; hepatotoxicity and nephrotoxicity may follow treatment with methotrexate or cyclosporine; teratogenicity is a risk of oral retinoids, and skin cancer may be caused by frequent PUVA (Psoralen and long wave ultraviolet radiation) treatments. [1],[2] In the past decade researchers have come up with new factors that may be involved in the pathogenesis of disease, but they have failed to establish a pathogenetic model that incorporates all the factors. There is a need to review our current concept and understanding of the pathogenesis of psoriasis. Lack of a clear pathogenetic mechanism especially in remissions, makes it very difficult to manage the disease on long term. This article is an attempt to bridge the gap that has come up with recent studies and to establish a better understanding of the pathogenesis of disease.

   T Cell Activation Top

It is widely believed that abnormal regulation of T cells coupled with interaction between keratinocytes and complex cytokine network is involved in the pathogenesis of the disease. [3],[4] In case the primary defect resides in keratinocytes, any physical or chemical injury to the defective keratinocytes could activate synthesis and release of cytokines thereby resulting in antigen-independent activation of T lymphocytes. This would further lead to release of additional cytokines followed by proliferation of keratinocytes, T lymphocytes and inflammation. Chang et al [5] have demonstrated that cytokines secreted by psoriatic epidermal cells potentiate T lymphocyte activation to a greater extent than cytokines secreted from normal epidermal cells. It is also postulated that only psoriatic keratinocytes respond to activated T cell messages with hyper-proliferation, because of their specific receptors or signal-transducing mechanisms [Figure 1]. [4] Further normal keratinocytes do not respond to psoriatic T cell supernatants. [6]

According to some studies the basement membrane (BM) structures are altered, and a complex network of cytokines, mainly Th1 type, are involved in various stages of pathogenesis. [1],[2],[3] Several new treatments reducing or eliminating the pathogenic effects of T cells are being investigated as possible anti psoriatic drugs. Alefacept binds to CD2 on T cells, blocking the LFA-3/CD2 interaction. [7] Alefacept also binds to FcgRIII IgG receptors on natural killer (NK) cells and macrophages, resulting in apoptosis of those T cells expressing high levels of CD2. Efalizumab is an antibody directed against the alpha subunit of LFA-1. [3],[4],[7] Etanercept and infliximab act as competitive inhibitors of tumour necrosis factor-alpha (TNF-α), which is an important pro-inflammatory cytokine in the pathobiology of psoriasis.[8],[9] Unfortunately, only one-third patients get significant benefit from the new and expensive immunomodulatory drugs. At least in the long term, increased risk of infection and possible reactivation of tuberculosis and lymphomas must be taken into account, as these new drugs are potentially immunosuppressive. [8]

   Hyperproliferation of Keratinocytes Top

The cell cycle time of hyperproliferating psoriatic keratinocytes is short. While maturation and shedding of keratinocytes takes 26 days in normal epidermis, it occurs in 4 days in psoriatic epidermis. [9] Growth factors, coming from various cell types, are believed to control the increased proliferation. Currently available antipsoriatic drugs act on keratinocyte proliferation. Calcipotriol, a vitamin D3 analog and retinoids, the natural and synthetic vitamin A derivatives, modulate keratinocyte hyperproliferation and differentiation. [10] Cyclosporine has strong antiproliferative effects on human epidermal keratinocytes in addition to immunomodulatory effects. [11]

   Angiogenesis Top

Keratinocytes are thought to be a major source of pro-angiogenic cytokines (VEGF, IL-8) but the precise mechanism for angiogenesis in psoriasis is still unknown. In a developing psoriatic plaque, endothelial cells swell and become activated showing prominent Golgi apparatus and Weibel-Palade bodies. [12] Activated endothelial cells migrate, sprout, and lay down a BM with pericytes for structural support to form novel vessel networks. [13] Activation and swelling of endothelial cells results in widening of the intercellular spaces, and dermal blood vessels dilate. The lesional capillary loops adopt a venous phenotype, including bridged fenestrations, and express E-selectin, making it easier for leukocytes to migrate into the skin. [14]

Although angiogenesis may not be the primary event in the pathogenesis of psoriasis, understanding the pathways leading to angio-proliferation may help in finding novel antipsoriatic drugs. [15] In fact, vitamin D analogues, retinoids, and cyclosporine all possess anti-angiogenic activity as well as antiproliferative and anti-inflammatory effects. [14],[16]

We could also accredit the impact of some environmental factors on the induction of psoriasis symptoms. Despite the clear familial aggregation of psoriasis, the precise inheritance model has been under debate. Currently, most investigators agree that psoriasis belongs to the group of complex diseases, the inheritance being multifactorial - genetic variants in multiple genes interact both with each other and the environment. [17],[18],[19],[20] Several disease susceptibility loci have been suggested as predisposing factors [21] [Table 1].

   Cytokine Mediators Top

Although a complex and multi-dimensional network of several cytokines has been found to be involved in pathobiology of psoriasis, none of these alone can be considered to be the causative. [35] [Table 2] shows some of the key cytokines involved in the pathogenesis of psoriasis.

Recently another chemokine CX3CL1 called Fractalkine (in humans) or neurotactin (in mice) has been identified in Psoriasis. CX3CL1 is produced as a long protein (with 373-amino acid in humans) with an extended mucin-like stalk and a chemokine domain on top. The mucin-like stalk permits it to bind to the surface of certain cells. However a soluble (90 kD) version of this chemokine has also been observed. Soluble CX3CL1 potently chemo-attracts T cells and monocytes, while the cell-bound chemokine promotes strong adhesion of leukocytes to activated endothelial cells, where it is primarily expressed. Fractalkine binding to its seven-transmembrane domain G protein coupled receptor CX3CR1 triggers signalling, but it also directly mediates cell adhesion. [63],[64] CX3CL1 is expressed within the brain, heart, lung, kidney, muscle and testis where it interacts with a single GPCR, CX3CR1 to trigger chemotaxis and adhesion of CX3CR1 expressing cells, including neutrophils, monocytes, NK cells and Th-1 polarized T cells. [65]

   Conclusion Top

For decades, the ongoing controversy on the molecular nature, choreography and hierarchy of these complex interactions e.g., between epidermal keratinocytes, T cells, neutrophils, endothelial cells and sensory nerves has served as a driving force propelling investigative dermatology to ever-new horizons. There is no question that advances in understanding the cellular immunology and biology of psoriasis, when coupled with the biotechnology revolution and rapid advances derived from human genetic studies of autoimmunity, have enhanced insights into the cause and treatment of psoriasis. The disease starts with the activation of T lymphocyte with an unknown antigen or gene product. T cell activation depends on its binding with APC (antigen presenting cell). T cells express the cell receptor known as TCR (T cell receptor), which recognizes the peptide being presented by the APC in the grove of MHC complex. The antigen stimulated activation leads to the conversion of naοve T-cells into an antigen specific cell, which may develop into a memory cell that circulate in the body [Figure 1]. After the activation of T cells, a cascade of cytokines viz. GMCSF (granulocyte macrophage colony stimulating factor), EGF, IL-1, IL-6, IL-8, IL-12, IL-17, IL-23, Fractalkine, TNF-α etc. are secreted by the activated T Cells. Due to effect of these cytokines there is keratinocyte proliferation, neutrophil migration, potentiation of Th-1 type response, angiogenesis, up-regulation of adhesion molecule and epidermal hyperplasia. We still lack a complete cure for this common and enigmatic disease, and we have not unequivocally identified genes or antigens responsible for its occurrence worldwide. Currently newer therapies are in pipeline, including an anti-IL23/22 fully humanized antibody, have also shown promise in treating psoriasis via both Th1 and Th17 pathways. But results of clinical trials will only prove its efficacy as long-term cure.

   References Top

1.Mehlis SL, Gordon KB. The immunology of psoriasis and biologic immunotherapy. J Am Acad Dermatol 2003;49:44-50.   Back to cited text no. 1    
2.Krueger JG, Bowcock A. Psoriasis pathophysiology: Current concepts of pathogenesis. Ann Rheum Dis 2005;64:ii30-6.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Ortonne JP. Recent developments in the understanding of the pathogenesis of psoriasis. Br J Dermatol 1999;140:54:1-7.   Back to cited text no. 3    
4.Bos JD, De Rie MA. The pathogenesis of psoriasis: Immunological facts and speculations. Immunol Today 1999;20:40-6.   Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Chang EY, Hammerberg C, Fisher G, Baadsgaard O, Ellis CN, Voorhees JJ, et al . T cell activation is potentiated by cytokines released by lesional psoriatic, but not normal, epidermis. Arch Dermatol 1992;128:1479-85.   Back to cited text no. 5  [PUBMED]  
6.Bata-Csorgo Z, Hammerberg C, Voorhees JJ, Cooper KD. Kinetics and regulation of human keratinocyte stem cell growth in short-term primary ex vivo culture: Cooperative growth factors from psoriatic lesional T lymphocytes stimulate proliferation among psoriatic uninvolved, but not normal, stem keratinocytes. J Clin Invest 1995;95:317-27.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Krueger GG, Callis KP. Development and use of alefacept to treat psoriasis. J Am Acad Dermatol 2003;49:S87-97.   Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Goffe B, Cather JC. Etanercept: An overview. J Am Acad Dermatol 2003;49:S105-11.   Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Gottlieb AB. Infliximab for psoriasis. J Am Acad Dermatol 2003;49:S112-7.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Hecker D, Lebwohl M. Topical calcipotriene in combination with UVB phototherapy for psoriasis. Int J Dermatol 1997;36:302-3.  Back to cited text no. 10  [PUBMED]  
11.Mondello MR, Califano L, Cannavo SP, Di Mauro D, Guarneri B, Magaudda L, et al . Psoriasis and cyclosporin: Immunohistochemical aspects of the basement membrane. Acta Derm Venereol Suppl 1994;186:96-8.   Back to cited text no. 11    
12.Christophers E, Mrowietz U. The inflammatory infiltrate in psoriasis. Clin Dermatol 1995;13:131-5.   Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Longo R, Sarmiento R, Fanelli M, Capaccetti B, Gattuso D, Gasparini G. Anti-angiogenic therapy: Rationale, challenges and clinical studies. Angiogenesis 2002;5:237-56.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Creamer D, Sullivan D, Bicknell R, Barker J. Angiogenesis in psoriasis. Angiogenesis 2002;5:231-6.   Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Nickoloff BJ. Characterization of lymphocyte-dependent angiogenesis using a SCID mouse: Human skin model of psoriasis. J Investig Dermatol Symp Proc 2000;5:67-73.   Back to cited text no. 15  [PUBMED]  
16.Olkawa T, Shimamura M, Ashino-Fuse H, Iwaguchi T, Ishizuka M, Takeuchi T. Inhibition of angiogenesis by 15-deoxyspergualin. J Antibiotics 1991;44:1033-5.  Back to cited text no. 16    
17.Farber EM, Nall ML. The natural history of psoriasis in 5600 patients. Dermatologica 1974;148:1-18.   Back to cited text no. 17  [PUBMED]  
18.Henseler T. Genetics of psoriasis. Arch Dermatol Res 1998;290:463-76.   Back to cited text no. 18  [PUBMED]  [FULLTEXT]
19.Elder JT, Nair RP, Henseler T, Jenisch S, Stuart P, Chia N, et al . The genetics of psoriasis 2001: The odyssey continues. Arch Dermatol 2001;137:1447-54.   Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Bowcock AM, Barker JN. Genetics of psoriasis: the potential impact on new therapies. J Am Acad Dermatol 2003;49:S51-6.   Back to cited text no. 20  [PUBMED]  [FULLTEXT]
21.Trembath RC, Clough RL, Rosbotham JL, Jones AB, Camp RD, Frodsham A, 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 1997;6:813-20.   Back to cited text no. 21  [PUBMED]  [FULLTEXT]
22.Nair RP, Henseler T, Jenisch S, Stuart P, Bichakjian CK, Lenk W, et al . Evidence for two psoriasis susceptibility loci (HLA and 17q) and two novel candidate regions (16q and 20p) by genome-wide scan. Hum Mol Genet 1997;6:1349-56.   Back to cited text no. 22  [PUBMED]  [FULLTEXT]
23.Jenisch S, Henseler T, Nair RP, Guo SW, Westphal E, Stuart P, et al . Linkage analysis of human leukocyte antigen (HLA) markers in familial psoriasis: Strong disequilibrium effects provide evidence for a major determinant in the HLA-B/-C region. Am J Hum Genet 1998;63:191-9.   Back to cited text no. 23  [PUBMED]  [FULLTEXT]
24.Enlund F, Samuelsson L, Enerback C, Inerot A, Wahlstrom J, Yhr M, et al . Psoriasis susceptibility locus in chromosome region 3q21 identified in patients from southwest Sweden. Eur J Hum Genet 1999;7:783-90.   Back to cited text no. 24    
25.Balendran N, Clough RL, Arguello JR, Barber R, Veal C, Jones AB, et al . Characterization of the major susceptibility region for psoriasis at chromosome 6p21.3. J Invest Dermatol 1999;113:322-8.   Back to cited text no. 25    
26.Samuelsson L, Enlund F, Torinsson A, Yhr M, Inerot A, Enerback C, et al . A genome-wide search for genes predisposing to familial psoriasis by using a stratification approach. Hum Genet 1999;105:523-9.   Back to cited text no. 26    
27.Oka A, Tamiya G, Tomizawa M, Ota M, Katsuyama Y, Makino S, et al . Association analysis using refined microsatellite markers localizes a susceptibility locus for psoriasis vulgaris within a 111 kb segment telomeric to the HLA-C gene. Hum Mol Genet 1999;8:2165-70.  Back to cited text no. 27  [PUBMED]  [FULLTEXT]
28.Tomfohrde J, Silverman A, Barnes R, Fernandez-Vina MA, Young M, Lory D, et al . Gene for familial psoriasis susceptibility mapped to the distal end of human chromosome 17q. Science 1994;264:1141-5.   Back to cited text no. 28  [PUBMED]  [FULLTEXT]
29.Matthews D, Fry L, Powles A, Weber J, McCarthy M, Fisher E, et al . Evidence that a locus for familial psoriasis maps to chromosome 4q. Nat Genet 1996;14:231-3.   Back to cited text no. 29  [PUBMED]  [FULLTEXT]
30.Bhalerao J, Bowcock AM. The genetics of psoriasis: A complex disorder of the skin and immune system. Hum Mol Genet 1998;7:1537-45.   Back to cited text no. 30  [PUBMED]  [FULLTEXT]
31.Capon F, Semprini S, Dallapiccola B, Novelli G. Evidence for interaction between Psoriasis susceptibility loci on chromosomes 6p21 and 1q21. Am J Hum Genet 1999;65:1798-800.  Back to cited text no. 31  [PUBMED]  [FULLTEXT]
32.Veal CD, Clough RL, Barber RC, Mason S, Tillman D, Ferry B, et al . Identification of a novel psoriasis susceptibility locus at 1p and evidence of epistasis between PSORS1 and candidate loci. J Med Genet 2001;38:7-13.   Back to cited text no. 32  [PUBMED]  [FULLTEXT]
33.Lee YA, Ruschendorf F, Windemuth C, Schmitt-Egenolf M, Stadelmann A, Nurnberg G, et al . Genomewide scan in german families reveals evidence for a novel psoriasis-susceptibility locus on chromosome 19p13. Am J Hum Genet 2000;67:1020-4.   Back to cited text no. 33    
34.Karason A, Gudjonsson JE, Upmanyu R, Antonsdottir AA, Hauksson VB, Runasdottir EH, et al . A susceptibility gene for psoriatic arthritis maps to chromosome 16q: Evidence for imprinting. Am J Hum Genet 2003;72:125-31.  Back to cited text no. 34  [PUBMED]  [FULLTEXT]
35.Bonifati C, Ameglio F. Cytokines in psoriasis. Int J Dermatol 1999; 38:241-51.  Back to cited text no. 35  [PUBMED]  [FULLTEXT]
36.Nickoloff BJ, Karabin GD, Barker JN, Griffiths CE, Sarma V, Mitra RS, et al . Cellular localization of interleukin-8 and its inducer, tumor necrosis factor-alpha in psoriasis. Am J Pathol 1991;138:129-40.   Back to cited text no. 36  [PUBMED]  [FULLTEXT]
37.Krueger JG. The immunologic basis for the treatment of psoriasis with new biologic agents. J Am Acad Dermatol 2002;46:1-23.  Back to cited text no. 37  [PUBMED]  [FULLTEXT]
38.Barker JN, Sarma V, Mitra RS, Dixit VM, Nickoloff BJ. Marked synergism between tumour necrosis factor-alpha and interferon-gamma in regulation of keratinocyte-derived adhesion molecules and chemotactic factors. J Clin Investig 1990;85:605-8.   Back to cited text no. 38  [PUBMED]  [FULLTEXT]
39.Kadunce DP, Krueger GG. Pathogenesis of psoriasis. Dermatol Clin 1995;13:723-37.   Back to cited text no. 39  [PUBMED]  
40.Werner S, Grose R. Regulation of wound healing by growth factors and cytokines. Physiol Rev 2002;83:835-70.   Back to cited text no. 40    
41.Werner S, Smola H. Paracrine regulation of keratinocyte proliferation and differentiation. Trends Cell Biol 2001;11:143-6.   Back to cited text no. 41  [PUBMED]  [FULLTEXT]
42.Lee RE, Gaspari AA, Lotze MT, Chang AE, Rosenberg SA. Interleukin 2 and psoriasis. Arch Dermatol 1988;124:1811-5.   Back to cited text no. 42  [PUBMED]  
43.Grossman RM, Krueger J, Yourish D, Granelli-Piperno A, Murphy DP, May LT, et al . Interleukin 6 is expressed in high levels in psoriatic skin and stimulates proliferation of cultured human keratinocytes. Proc Natl Acad Sci USA 1989;86:6367-71.   Back to cited text no. 43  [PUBMED]  [FULLTEXT]
44.Gillitzer R, Ritter U, Spandau U, Goebeler M, Brocker EB. Differential expression of GROalpha and IL-8 mRNA in psoriasis: A model for neutrophil migration and accumulation in vivo. J Invest Dermatol 1996;107:778-82.  Back to cited text no. 44    
45.Nickoloff BJ, Mitra RS, Varani J, Dixit VM, Polverini PJ. Aberrant production of interleukin-8 and thrombospondin-1 by psoriatic keratinocytes mediates angiogenesis. Am J Pathol 1994;144:820-8.   Back to cited text no. 45  [PUBMED]  [FULLTEXT]
46.Nanney LB, Stoscheck CM, Magid M, King LE Jr. Altered epidermal growth factor binding and receptor distribution in psoriasis. J Invest Dermatol 1986;86:260-5.  Back to cited text no. 46  [PUBMED]  
47.Krane JF, Gottlieb AB, Carter DM, Krueger JG. The insulin-like growth factor I receptor is overexpressed in psoriatic epidermis, but is differentially regulated from the epidermal growth factor receptor. J Exp Med 1992;175:1081-90.   Back to cited text no. 47  [PUBMED]  [FULLTEXT]
48.Kirby B, Griffiths CE. Psoriasis: The future. Br J Dermatol 2001;144:37-43.   Back to cited text no. 48  [PUBMED]  [FULLTEXT]
49.Detmar M, Brown LF, Schon MP, Elicker BM, Velasco P, Richard L, et al . Increased microvascular density and enhanced leukocyte rolling and adhesion in the skin of VEGF transgenic mice. J Invest Dermatol 1998;111:1-6.   Back to cited text no. 49    
50.Yaguchi H, Tsuboi R, Ueki R, Ogawa H. Immunohistochemical localization of basic fibroblast growth factor in skin diseases. Acta Dermatol Venereol 1993;73:81-3.   Back to cited text no. 50    
51.Pincelli C. Nerve growth factor and keratinocytes: A role in psoriasis. Eur J Dermatol 2000;10:85-90.   Back to cited text no. 51  [PUBMED]  [FULLTEXT]
52.Raychaudhuri SP, Raychaudhuri SK. Role of NGF and neurogenic inflammation in the pathogenesis of psoriasis. Prog Brain Res 2004;146:433-7.   Back to cited text no. 52  [PUBMED]  
53.Davenport AP. International union of pharmacology, XXIX: Update on endothelin receptor nomenclature. Pharmacol Rev 2002;54:219-26.  Back to cited text no. 53  [PUBMED]  [FULLTEXT]
54.Lee E, Trepicchio WL, Oestreicher JL, Pittman D, Wang F, Chamian F, et al . Increased expression of interleukin 23 pl 19 and p40 in lesional skin of patients with psoriasis vulgaris. J Exp Med 2004;199:125-30.  Back to cited text no. 54  [PUBMED]  [FULLTEXT]
55.Harington LE, Hatton RD, Mangan PR, Turner H, Murphy TL, Murphy KM, et al . Interleukin 17- producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat Immunol 2005;6:1123-32.  Back to cited text no. 55    
56.Piskin G, Sylva-Streenland RM, Bos JD, Teunissen MB. In vitro and in situ expression of IL-23 by Keratinocyte in healthy skin and psoriasis lesions: Enhanced expression in psoriatic skin. J Immunol 2006;176:1908-15.  Back to cited text no. 56    
57.Pilcher BK, Dumin JA, Sudbeck BD, Krane SM, Welgus HG, Park WC. The activity of collogenase-1 is required for Kerationocyte migration on a type 1 collagen matrix. J Cell Biol 1997;137:1445-57.  Back to cited text no. 57    
58.Watson PH, Leygne ER, Murphy LC. Psoriasin (S100A7). Int J Biochem Cell Biol 1998;30:567-71.  Back to cited text no. 58    
59.Broome AM, Ryan D, Eckert RL. S100 protein sub-cellular localization during epidermal differentiation and psoriasis. J Histochem Cytochem 2003;51:675-85.  Back to cited text no. 59  [PUBMED]  [FULLTEXT]
60.Stark MA, Huo Y, Burcin TL, Morris MA, Olson TS, Ley K. Phagocytosis of apoptotic neutrophils regulates granulopoiesis via IL-23 and IL-17. Immunity 2005;22:285-94.  Back to cited text no. 60  [PUBMED]  [FULLTEXT]
61.Numasaki M, Fukushi J, Ono M, Narula SK, Zavodny PJ, Kudo T, et al . Interleukin-17 promotes angiogenesis and tumor growth. Blood 2003;101:2620-7.  Back to cited text no. 61  [PUBMED]  
62.Komiyama Y, Nakae S, Matsuki T, Nambu A, Ishigame H, Kakuta S, et al . IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis. J Immunol 2006;177:566-73.  Back to cited text no. 62  [PUBMED]  [FULLTEXT]
63.Imai T, Hieshima K, Haskell C, Baba M, Nagira M, Nishimura M, et al . Identification and molecular characterization of fractalkine receptor CX3CR1, which mediates both leukocyte migration and adhesion. Cell 1997;91:521-30.  Back to cited text no. 63  [PUBMED]  [FULLTEXT]
64.Fong AM, Robinson LA, Steeber DA, Tedder TF, Yoshie O, Imai T, et al . Fractalkine and CX3CR1 mediate a novel mechanism of leukocyte capture, firm adhesion and activation under physiologic flow. J Exp Med 1998;188:1413-9.  Back to cited text no. 64  [PUBMED]  [FULLTEXT]
65.Haskell CA, Cleary MD, Charo IF. Molecular uncoupling of fractalkine-mediated cell adhesion and signal transduction: Rapid flow arrest of CX3CR1-expressing cells is independent of G-protein activation. J Biol Chem 1999;274:10053-8.  Back to cited text no. 65  [PUBMED]  [FULLTEXT]


  [Figure 1]

  [Table 1], [Table 2]

This article has been cited by
1 Effects of Cyclosporine A and Adalimumab on the expression profiles histaminergic system-associated genes and microRNAs regulating these genes in HaCaT cells
Tomasz Kasela, Maciej Dabala, Magdalena Mistarz, Weronika Wieczorek, Magdalena Wierzbik-Stronska, Kacper Boron, Barbara Zawidlak-Wegrzynska, Beniamin Oskar Grabarek
Cell Cycle. 2022; : 1
[Pubmed] | [DOI]
2 Nanotechnology-based Medicinal Products and Patents: A Promising Way to Treat Psoriasis
Faraat Ali, Kumari Neha, Kamna Sharma, Shaik Khasimbi, Garima Chauhan
Current Drug Delivery. 2022; 19(5): 587
[Pubmed] | [DOI]
3 Effect of Melatonin on Psoriatic Phenotype in Human Reconstructed Skin Model
Sarah Adriana Scuderi, Laura Cucinotta, Alessia Filippone, Marika Lanza, Michela Campolo, Irene Paterniti, Emanuela Esposito
Biomedicines. 2022; 10(4): 752
[Pubmed] | [DOI]
4 Nanoemulsions: A Review on the Conceptualization of Treatment for Psoriasis Using a ‘Green’ Surfactant with Low-Energy Emulsification Method
Ignatius Julian Dinshaw, Noraini Ahmad, Norazlinaliza Salim, Bey Fen Leo
Pharmaceutics. 2021; 13(7): 1024
[Pubmed] | [DOI]
5 Management of psoriasis in children (Review)
Daciana Branisteanu, Simona Georgescu, Ionela Serban, Alin Pinzariu, Daniel Boda, Minela Maranduca, Mihai Glod, Catalina Branisteanu, Roxana Bilibau, Andreea  Dimitriu, Alin Nicolescu, Daniel Branisteanu
Experimental and Therapeutic Medicine. 2021; 22(6)
[Pubmed] | [DOI]
6 Natural and Nanotechnology Based Treatment: An Alternative Approach to Psoriasis
Nishu Yadav, Rohan Aggarwal, Monika Targhotra, Prabhat K. Sahoo, Meenakshi K. Chauhan
Current Nanomedicine. 2021; 11(1): 21
[Pubmed] | [DOI]
7 Immunomodulators in the Treatment of Psoriasis
Namitha Maniyan, K. Sreejith, Cherakkulath C Neena, B. Athulnadh, P.P. Muhamed Faris, K.V. Musaina Thasneem, K Gayathri
Journal of Drug Delivery and Therapeutics. 2020; 10(6): 213
[Pubmed] | [DOI]
8 Tackling the various classes of nano-therapeutics employed in topical therapy of psoriasis
Salma A. Fereig, Ghada M. El-Zaafarany, Mona G. Arafa, Mona M. A. Abdel-Mottaleb
Drug Delivery. 2020; 27(1): 662
[Pubmed] | [DOI]
9 Psoriatic disease and body composition: A systematic review and narrative synthesis
Tim Blake, Nicola J. Gullick, Charles E. Hutchinson, Thomas M. Barber, Michael Nurmohamed
PLOS ONE. 2020; 15(8): e0237598
[Pubmed] | [DOI]
10 Retinoic Acid and Its Derivatives in Skin
Lukasz Szymanski, Rafal Skopek, Malgorzata Palusinska, Tino Schenk, Sven Stengel, Slawomir Lewicki, Leszek Kraj, Pawel Kaminski, Arthur Zelent
Cells. 2020; 9(12): 2660
[Pubmed] | [DOI]
11 Genome-Wide DNA Methylation Profiling Identifies Differential Methylation in Uninvolved Psoriatic Epidermis
Deepti Verma, Anna-Karin Ekman, Cecilia Bivik Eding, Charlotta Enerbäck
Journal of Investigative Dermatology. 2018; 138(5): 1088
[Pubmed] | [DOI]
12 Serum Paraoxonase Levels in Type 2 Diabetes Mellitus Patients: A Case-Control Study
D Namitha, Aliya Nusrath, A Rajeshwari, N Asha Rani
Journal of Medical Sciences and Health. 2015; 01(02): 14
[Pubmed] | [DOI]
13 Prolonged remission of psoriasis with azathioprine pulse therapy
Ramji Gupta
Apollo Medicine. 2014; 11(3): 213
[Pubmed] | [DOI]
14 Azathioprine Pulse Therapy in the treatment of psoriatic arthritis: A case series
Ramji Gupta
Apollo Medicine. 2014;
[Pubmed] | [DOI]
15 Whole-genome DNA methylation in skin lesions from patients with psoriasis vulgaris
Peng Zhang,Ming Zhao,Gongping Liang,Guangliang Yin,Dan Huang,Fengxia Su,Hanyue Zhai,Litao Wang,Yuwen Su,Qianjin Lu
Journal of Autoimmunity. 2013; 41: 17
[Pubmed] | [DOI]
16 Whole-genome DNA methylation in skin lesions from patients with psoriasis vulgaris
Zhang, P. and Zhao, M. and Liang, G. and Yin, G. and Huang, D. and Su, F. and Zhai, H. and Wang, L. and Su, Y. and Lu, Q.
Journal of Autoimmunity. 2013; 41: 17-24
17 Morphometric study of microvessels, epidermal characteristics and inflammation in psoriasis vulgaris with their correlations
Boruah, D. and Moorchung, N. and Vasudevan, B. and Malik, A. and Chatterjee, M.
Indian Journal of Dermatology, Venereology and Leprology. 2013; 79(2): 216-223
18 Role of NF-?B in the pathogenesis of psoriasis elucidated by its staining in skin biopsy specimens
Nikhil Moorchung,Janmeet S. Kulaar,Manas Chatterjee,Biju Vasudevan,Tanu Tripathi,Vibha Dutta
International Journal of Dermatology. 2013; : n/a
[Pubmed] | [DOI]
19 The Association Between Psoriasis and Cardiovascular Diseases
Göknur Kalkan, A. Serap Karadag
Electronic Journal of General Medicine. 2013; 10(Supplement): 10
[Pubmed] | [DOI]
20 Serum neopterin and TNF-α levels in psoriasis and their correlation with disease severity [Psoriasisde serum neopterin ve TNF-α düzeyleri ve hastalik şiddeti ile i̇lişkisi]
Ceyhan, A.M. and Yildirim, M. and Ceyhan, B.M. and Sütçü, R.
Turkderm Deri Hastaliklari ve Frengi Arsivi. 2012; 46(1): 7-10
21 Serum neopterin and TNF-α levels in psoriasis and their correlation with disease severity | [Psoriasisde serum neopterin ve TNF-α düzeyleri ve hastalik şiddeti ile i̇lişkisi]
Ceyhan, A.M., Yildirim, M., Ceyhan, B.M., Sütçü, R.
Turkderm Deri Hastaliklari ve Frengi Arsivi. 2012; 46(1): 7-10
22 Reviewing concepts in the immunopathogenesis of psoriasis [Imunopatogênese da psoríase: Revisando conceitos]
Lima, E.A. and Lima, M.A.
Anais Brasileiros de Dermatologia. 2011; 86(6): 1151-1158
23 Clinical observation of TGP in the treatment of psoriasis vulgaris
Zhang, Y.-H., Guo, Z.-P., Jiao, X.-Y., Chen, T.
Journal of Clinical Dermatology. 2011; 40(7): 433-435
24 Reviewing concepts in the immunopathogenesis of psoriasis | [Imunopatogênese da psoríase: Revisando conceitos]
Lima, E.A., Lima, M.A.
Anais Brasileiros de Dermatologia. 2011; 86(6): 1151-1158
25 Cardiovascular comorbiditiy in psoriasis
Singh, G., Aneja, S.P.S.
Indian Journal of Dermatology. 2011; 56(5): 553-556


Print this article  Email this article
   Next article
   Previous article 
   Table of Contents
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (400 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  

    T Cell Activation
    Cytokine Mediators
    Article Figures
    Article Tables

 Article Access Statistics
    PDF Downloaded1356    
    Comments [Add]    
    Cited by others 25    

Recommend this journal