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Year : 2013  |  Volume : 40  |  Issue : 3  |  Page : 121-127

Update on Psoriasis

1 Department of Oral Pathology and Microbiology, D.J. College of Dental Sciences and Research, Modinagar, Ghaziabad, Uttar Pradesh, India
2 Department of Prosthodontics, D.J. College of Dental Sciences and Research, Modinagar, Ghaziabad, Uttar Pradesh, India

Date of Web Publication19-Oct-2013

Correspondence Address:
Robin Sabharwal
Department of Oral Pathology and Microbiology, D.J. College of Dental Sciences and Research, Ajit Mahal, Niwari Road, Modinagar, Ghaziabad - 201 204, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0974-5009.120039

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Psoriasis is a common skin disorder characterized by focal formation of raised plaques that constantly shed scales derived from excessive growth of skin epithelial cells. The disease is characterized by a series of linked cellular changes in the skin: hyperplasia of epidermal keratinocytes, vascular hyperplasia and ectasia, and infiltration of T lymphocytes, neutrophils, and other types of leukocyte in the affected skin. Psoriasis is now considered as a T cell-mediated inflammation of the skin. Types of psoriasis that may be clinically encountered include plaque psoriasis, guttate psoriasis, erythrodermic psoriasis, pustular psoriasis, nail psoriasis, psoriatic arthritis, and scalp psoriasis. Psoriasis is believed to be genetically linked but can also be triggered by mechanical, ultraviolet, and chemical injury; various infections; prescription drug use; psychological stress; smoking; and other factors.

Keywords: Langerhans cells, psoriasis, T cell activation

How to cite this article:
Puri A, Sengupta S, Sharma B, Sabharwal R, Kapoor K. Update on Psoriasis. J Sci Soc 2013;40:121-7

How to cite this URL:
Puri A, Sengupta S, Sharma B, Sabharwal R, Kapoor K. Update on Psoriasis. J Sci Soc [serial online] 2013 [cited 2020 Sep 22];40:121-7. Available from: http://www.jscisociety.com/text.asp?2013/40/3/121/120039

  Introduction Top

Psoriasis is a chronic skin disease affecting about 1.5-3% of the world's population, [1] although usually not life-threatening, but causes tremendous morbidity and has no cure. Although psoriasis has been ubiquitous through the ages, it was not until the end of the 18 th century that it was first described as a separate skin disorder. [2] Classic psoriasis is characterized by abnormal cycle of epidermal development that leads to epidermal hyperproliferation, altered maturation of the skin, inflammation, and vascular alterations. [3] These four characteristics are often observed as areas of dry, thickened, scaling, silvery white, and reddened skin. [4] With recent developments in understanding the role of inflammation in the pathogenesis of psoriasis, it is now widely believed that psoriasis is not just a skin disease but a systemic inflammatory process. Along with skin problems it has an increased risk of other chronic disorders including diabetes mellitus, hypertension, coronary artery disease, fatigue, and depression.

Clinical features

Psoriasis derives its name from the Greek word 'psora', which means 'itch'. It is commonly seen in the second or third decade of life with a slight predilection in females and tends to persist for years with periods of exacerbation and quiescence. The lesions usually improve during the summer and worsen in the winter, which may be related to lesional exposure to ultraviolet light. The lesions are often symmetrically distributed in certain preferential locations such as the scalp, elbows, and knees. The lesions appear as well-demarcated, erythematous (salmon pink), indurated plaque, dry papules, each covered by a delicate silvery scale on its surface resembling a thin layer of mica with peripheral blanching (Woronoff's sign). The lesions are typically asymptomatic but, occasionally, the patient complains of itching, erythema, and pruritis; moreover, bleeding points can occur when the patient scratches the lesions (Auspitz sign). The inflammation involving the skin can be accompanied by arthritis, and the joint disease is present in about one-third of psoriatic patients. An unfortunate complication affecting approximately 4% of these patients is psoriatic arthritis (PsA), which may involve the temporomandibular joint.

Oral manifestations

Oral lesions can occur on the mucous membranes of the mouth, but it is not as common as on the skin and are usually accompanied by lesions on other parts of the body. [5] Reports of oral psoriasis that are well documented show no consistent lesion pattern. Patterns range from raised, white, scaling lesions predominantly on the palate or buccal mucosa to well-demarcated, flattened, erythematous lesions involving the dorsal surface of the tongue with a slightly raised, white, and annular or serpiginous border. These latter lesions closely resemble geographic tongue. Oral lesions may disappear quickly or they may undergo exacerbations or remissions concomitantly with skin lesions. Diagnosis of oral psoriasis is best made when the clinical course of the oral lesion parallels that of the skin disease and is supported by microscopic findings. [6]

Clinical types

From a clinical perspective, the inflammatory process in the skin can manifest itself with many different types of presentations, ranging from the small tear-shaped skin lesions known as guttate psoriasis to pustular forms and generalized erythrodermic variants, besides the classic thick, well-demarcated erythematous plaques. [5] Several types of psoriatic lesions may occur [Table 1]; each differs slightly and responds differently to treatment. The most common form is plaque psoriasis, which occurs in about 90% of patients. [7]
Table 1: Different clinical types of psoriasis with their characteristics

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The triggering factors for the onset or exacerbation of the disease are highly varied, ranging from a bacterial pharyngitis (usually caused by gram-positive bacteria) to mechanical, ultraviolet, or chemical injury of the skin (Koebner's phenomenon). The psoriatic lesions reflect the physical pattern of epidermal injury; various infections (especially streptococcal infections, but also acute viral infections and HIV infection); drug use such as antimalarials, lithium, β-blockers, quinidine, systemic corticosteroids (upon withdrawal), and indomethacin; psychological stress; endocrine and hormonal changes; obesity; alcohol; and smoking.[7] In many patients, the disease is inherited, but the precise identification of genetic susceptibility loci contributing to disease pathogenesis remains to be determined. Two noteworthy features of psoriasis must be taken into consideration; first, the lesions are entirely reversible, and the diseased skin can, either spontaneously (rarely) or after effective therapy, be restored to a normal state without scarring. Second, despite the chronic inflammatory reaction, it is rare for a psoriatic plaque to be converted to a malignant squamous cell carcinoma. Thus, it appears that in the course of creating a psoriatic plaque, a field effect is established that imbues the tissue with a remarkable tumor suppressor-like quality. [5]


Psoriasis has since long been considered a hyperproliferative skin disease with a markedly increased (5-6 times normal) rate of epidermal turnover. This, along with the invariable presence of neutrophils within the epidermis of psoriatic lesions, led to the thinking that abnormalities of the epidermis are central to the pathogenesis of psoriasis. [8] Role of T cells, antigen-presenting cells (APCs), keratinocytes, Langerhans cell, macrophages, natural killer cells, an array of Th1-type cytokines, as well as certain growth factors like vascular endothelial growth factor (VEGF), keratinocytes growth factor (KGF), etc have been suggested to play a key in the pathogenesis of psoriasis. [9] But now it is well accepted that psoriasis is in fact an immunologically mediated disease where activation of T lymphocytes is central to the inflammation in the dermal microenvironment and also that epidermal hyperproliferation is secondary to the inflammatory events that follow the most common Th1 type of immunological skin disease. [10]

Various mechanisms are hypothesized to be involved in the pathogenesis of psoriasis:

  • T cell function
  • Role of dendritic cell
  • Hyperproliferation of keratinocytes
  • Angiogenesis
  • Cytokine mediators
  • Reduced apoptosis
  • Genetic factors
  • Role of oxidants and antioxidants in psoriasis
1. T cell function

T lymphocytes consist of a functionally distinct population of helper T cells and cytolytic T cells. The principal function of T cells is to regulate all immune responses to protein antigens. T cells, unlike B lymphocytes, do not produce antibodies but recognize only processed peptide antigens that are attached to proteins encoded by the MHC class II genes. Therefore, for activation, T cells need APCs to process and present peptide fragments on the APC cell surface. T cells respond to only cell surface - associated antigens and not to soluble antigens. On appropriate stimulation, T cells secrete various lymphokines. T cells may also inhibit immune responses; in this role, these are known as suppressor T cells.

Functionally different populations of T cells express distinct cell membrane proteins that serve as phenotypic markers for different lymphocyte populations. Most helper T cells express CD4, while cytolytic and suppressor cells are CD8 positive. CD (cluster of differentiation) refers to a molecule on the cell surface that is recognized by a cluster of monoclonal antibodies, and which can be used to identify the lineage of or the stage of differentiation of lymphocytes.

Activation of T cells requires three steps [8] :

  1. Binding
  2. Antigen-specific activation (signal 1)
  3. Non-antigen - specific cell-cell interaction (signal 2)
a. Binding

The T cell attaches to the APC through surface adhesion molecules, which are located reciprocally on the cell surfaces of both the T cells and the APCs. The leukocyte function associated antigen 1 (LFA-1) and CD2 are adhesion molecules of T lymphocytes that attach to reciprocating adhesion molecules expressed on the surface of APCs (intercellular adhesion molecule, ICAM-1; and LFA-3) [Figure 1]. In the skin, Langerhans cell is the most efficient APC. [8]
Figure 1: T cell activation depends on its binding with APC.

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b. Antigen-specific activation

Once the T cell-APC binding has occurred through their respective surface adhesion molecules, the antigen is presented to the T cell by the APC [Figure 2]. T cells express the T cell receptors (TCR), which recognizes the peptide antigen being presented by the APC in the groove of MHC complex. This antigen-stimulated activation leads to conversion of a native T cell into an antigen-specific cell that may further develop into a long-lived memory cell circulating in the body and can recognize the same antigen at a later date, even after several years. [8]
Figure 2: Activation of T lymphocyte with an unknown antigen.

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c. Non-antigen - specific cell-cell interaction

This is also known as co-stimulation. If co-stimulation by other cell surface molecules does not occur following antigen presentation, the T cell will not respond to the antigen and will undergo apoptosis or be rendered unresponsive to that antigen in the future. [8]

Once the T cell is activated, the next step is induction of inflammatory responses and release of cytokines by the activated T cells [Figure 3]. The stimulation of both TCR and CD28 pathways leads to transcription of interleukin (IL)-2, tumor necrosis factor-alpha (TNF-α), granulocyte - macrophage colony stimulating factor (GM-CSF), and interferon-alpha (IFN-γ), leading to keratinocyte proliferation, neutrophil migration, angiogenesis, and upregulation of adhesion molecule and epidermal hyperplasia, these tissue changes leadto clinical picture of psoriasisMany cell types are involved in this final step (T cells, macrophages, dendritic cells, vascular endothelium, and keratinocytes). 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. [11]
Figure 3: Non-antigen - specific cell-cell interactions (co-stimulation).

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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. It has been demonstrated that cytokines secreted by psoriatic epidermal cells potentiate T lymphocytes 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. [12] Furthermore, normal keratinocytes do not respond to psoriatic T cell supernatants. [9]

1. Role of dendritic cells

Dendritic cells form another major class of leucocytes that is found in increased abundance in psoriatic skin lesions. [13] Langerhans cells, considered as a type of immature dendritic cell (iDC), are resident in normal epidermis and can also be found in psoriasis lesions, sometimes in increased abundance. [14] It is likely that iDCs are derived from blood monocytes or other myeloid precursors and that these cells can be further stimulated to become mature DCs (mDCs) - cells that have potent immunostimulatory capacity for T lymphocytes. Psoriasis lesions show a marked increase in dermal DCs. XIIIa and CD11c expression is used as one of the most consistent markers of myeloid DCs or iDCs, and the best marker of mDC is expression of CD83 and DC-LAMP proteins; moreover, many CD83+ and DC-LAMP+ mDCs are present in the epidermis and dermis of psoriasis lesions based on immunophenotyping. Therefore, mDCs are considered to be potent stimulators of T cells. Finally, another type of DC termed as plasmacytoid DC (pDC) dramatically increases in psoriatic skin. Although pDCs are a minor DC subset in skin lesions, they have the ability, if activated, to produce extremely large amounts of IFN-α. In contrast, activated/mature myeloid DCs are known to be major producers of IL-12 and IL-23, and thus strong polarizers of T cell responses. [15],[16]

2. Hyperproliferation of keratinocytes

The main function of the skin is to offer protection through an intact epidermal layer. The epidermis consists of five layers, which are, from the deepest to most superficial, stratum basale, stratum spinosum, stratum granulosum, stratum lucidium, and stratum corneum. Four types of cells compose these layers: keratinocytes (90% of the cells), melanocytes (8%), Langerhans cells, and tactile menisci (also known as Merkel cells). During the epidermal cell cycle, new cells formed in the stratum basale migrate toward the stratum corneum. As cells move toward the surface, they accumulate keratin and their organelles disappear. By the time the cells reach the stratum corneum, they are dead and completely filled with keratin. This smooth, keratinous external layer is what offers the skin its protection. The surface cells slough off (exfoliate) and are replaced by underlying cells. The epidermal cell cycle normally takes about four weeks. Keratinocytes in the basal layer divide approximately once every two weeks. [17]

In psoriatic skin, the epidermal cell cycle is accelerated. Cell division in the basal layer occurs every 1.5 days, and the migration of keratinocytes to the stratum corneum occurs within approximately four days. Since the cells move to the surface so rapidly, they are unable to differentiate and mature properly. Hence, squamous keratinocytes aberrantly retain intact nuclei (parakeratosis) and release few extracellular lipids that normally cement the adhesion of corneocytes. This results in formation of poorly adherent stratum corneum, and thus, the characteristic scales or flakes of psoriatic lesions.

The epidermis in psoriatic lesions is 3-5 times thicker than normal. Blood vessels in the papillary layer of the dermis dilate in psoriasis, and inflammatory cells, such as neutrophils, infiltrate the epidermis. [7]

3. Angiogenesis

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. [18] Activated endothelial cells migrate, sprout, and lay down a basement membrane with pericytes for structural support to form novel vessel networks. [19] Activation and swelling of endothelial cells result in widening of the intercellular spaces, and hence, 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. [20]

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. In fact, vitamin D analogues, retinoids, and cyclosporine all possess anti-angiogenic activity as well as antiproliferative and anti-inflammatory effects. [21]

4. Cytokine mediators

In psoriasis, it is likely that a cascade of cytokines are secreted by different cells in the local microenvironment and play a role leading to the typical phenotypic responses seen in psoriasis, namely, vascular dilatation, dermal inflammation, and resultant hyperproliferation of the epidermis. The cytokines involved in the development of psoriasis include granulocyte-macrophage colony stimulating factor (GMCSF), epithelial growth factor (EGF), IL-8, IL-12, IL-1, IL-6, IFN-γ, and TNF-α. The effects of these cytokines include keratinocyte proliferation, neutrophil migration, potentiation of Th1 type of responses, angiogenesis, upregulation of adhesion molecules, and epidermal hyperplasia. TNF-α is strongly implicated in the pathogenesis of psoriasis and PsA. It plays a critical role in activation of innate and acquired immune responses leading to chronic inflammation, tissue damage, and keratinocyte proliferation. TNF-α functions in a positive feedback loop by recruiting more inflammatory cells and upgrading receptors on those cells. TNF-α levels are markedly increased in skin lesions, synovium, and serum of patients with psoriasis, and these are correlated with the severity of the disease. [8]

In the Th-1cytokine network immune response, the net effect of producing IL-2, IFN-γ, and TNF-α was to promote a T cell-mediated reaction. Conversely, in the TH-2 cytokine network response, the net immune response included IL-3, IL-4, IL-5, and IL-10 contributing to a humoral or B cell-mediated immune reaction. [16]

Interleukin 12 is a heterodimer composed of p40 and p35 subunits that is produced by activated macrophages and dendritic cells. Interleukin 12 is a strong inducer of a TH-1-type differentiation response with native T cells becoming IFN-γ-producing T cells. Interleukin 23 is a heterodimer composed of p40 and p19 subunits that is also produced by activated mononuclear cells leading to memory TH-1-type T cells. An antibody that recognizes the shared subunit (eg, p40) has been found to induce clinical responses in psoriatic patients. [22]

Besides TH-1- vs TH-2-type immune system, there is also a cytokine network highlighted by the dominance of a TH-17-type response. The cytokine at the center of this new and emerging paradigm, IL-17, may be important in psoriasis because it can promote accumulation of neutrophils and impact barrier function. [23],[24] Recent studies implicate protein kinase C α-mediated signaling in psoriatic lesions, thereby linking TNF-α, nuclear factor-κB, and chemotactic factors in the inflammatory process culminating in conversion of prepsoriatic skin to psoriatic plaques. [25],[26]

5. Reduced apoptosis

Proliferation of keratinocytes in normal epidermis is regulated by apoptotic cell death in order to maintain a constant thickness of the epidermis. The epidermal hyperplasia characteristic of psoriasis is suggested to be due to aberrant epidermal expression of apoptosis-related molecules leading to suppression of the apoptotic process. Apoptosis is controlled genetically where P53 and Bcl-2 play a central role in its regulation. The normal or wild-type P53 protein acts as a potent suppressor of cell growth and is upregulated in response to a variety of DNA-damaging agents resulting in apoptosis. In psoriasis, many investigators reported overexpression of P53 in the keratinocytes of both psoriatic and non-lesional skin, with higher expression of P53 in lesional than in non-lesional skin. Therefore, P53 overexpression can be explained as a physiological reaction to the hyperproliferation. Also, the actively proliferating cells typically express Bcl-2 that protects them against apoptotic stimuli, while terminally differentiated cells lose Bcl-2 expression. [27]

6. Genetic factor

It is currently believed that psoriasis is a genetically linked disease and may be carried on more than one gene. About 30% of people affected with the disease had psoriasis in their family. [28] It has an autosomal dominant pattern of inheritance. If one parent has the disease, there is a 25% chance that his or her offspring will also get the disease; if both parents are carriers, the chance of passing psoriasis on to their children more than doubles. [29] The frequency of psoriasis is higher in monozygotic than dizygotic twins. [28] In many types of psoriatic patients, levels of human leukocyte antigens (HLAs) are above normal, indicating a genetic predisposition favoring activation of psoriasis. Not all persons with abnormal HLA presentation will become psoriatic in the future, but there is a notable increase in risk. [30]

Psoriasis and associated PsA are complex genetic diseases with both environmental and genetic components. Approximately 10-30% of patients with psoriasis develop PsA. This suggests that susceptibility factors for psoriasis are also susceptibility factors for PsA. However, the development of PsA in psoriasis patients may require additional environmental stimuli or additional genetic factors that predispose to inflammation of the joints as well as the skin. Susceptibility loci for psoriasis reside on chromosomes 1q21, 3q21, 4q, 7p, 8, 11, 16q, 17q, and 20p. Recently, two regions on chromosome 17q were precisely localized with association mapping. These regions are separated by 6 Mb so that their contribution to psoriasis susceptibility appears to be independent. Some of the genes involved are SLC9A3R, NAT9, RUNX1, and RAPTOR. [16]

7. Role of oxidants and antioxidants in psoriasis

The role of oxidants and antioxidants in the pathogenesis of psoriasis can be explained by three factors:-

  1. Role of antioxidant system
  2. Role of heme oxygenase
  3. Role of nitric oxide
a. Role of anti-oxidant system

The skin is constantly exposed to endogenous and environmental pro-oxidant agents, which lead to harmful generation of reactive oxygen species (ROS). Healthy skin, being a potential target for oxidative stress, is equipped with a large number of defence mechanisms including antioxidant systems. This protection can be corrupted due to an imbalance between ROS and antioxidants with pathological level of oxidants prevailing. There is a great body of evidence indicating that some inflammatory skin diseases, such as psoriasis, are mediated by oxidative stress. Keratinocytes of normal skin, the primary target for pro-oxidant agents, show strong expression of ROS-detoxifying enzymes. While in psoriatic lesions, ROS are generated by both keratinocytes and activated inflammatory cells, mostly neutrophils. In such conditions, when natural antioxidant defence systems are overwhelmed by a prolonged production of ROS, the resulting oxygen free radicals damage proteins, lipids, and DNA. It is suggested that increased production of ROS and deficient function of antioxidant systems may be involved in the pathogenesis of psoriasis. [31]

b. Role of Heme oxygenase

In addition, normal keratinocytes express heme oxygenase (HO), an enzyme that might be involved in the protection of cells against oxidative stress. HO (inducible HO-1, constitutive HO-2 and HO-3) is the rate-limiting enzyme in heme catabolism, which leads to the generation of biliverdin, iron, and carbon monoxide. HO-1 is a stress-responsive protein whose expression is induced by various oxidative agents. HO-1 is known for its cytoprotective, antioxidant, and anti-inflammatory properties. Interestingly, a strong overexpression of HO-1 was observed in psoriatic skin. [31]

In epidermal cells, hydrogen peroxide (H 2 O 2 ) levels increase in response to a variety of pro-oxidant agents such as UVA radiation, sun light, and in response to free iron, liberated from storage (ferritin) and heme-containing proteins. Heme oxygenase, the heme degrading enzyme, represents an important mechanism of protective response to oxidative cellular stress. HO-2 and HO-3 isoenzymes are constitutively expressed and function mainly in normal heme capturing and metabolism. The inducible HO-1 isoform is known to be involved in wound repair and in the resolution of inflammatory response. HO converts heme into biliverdin/bilirubin, free divalent iron, and carbon monoxide (CO). Biliverdin and bilirubin function as a potent antioxidant system, whereas CO exerts anti-inflammatory activities. Furthermore, the iron released from heme enhances ferritin synthesis, and thereby renders it inactive by sequestering. However, during the inflammatory process, free iron may be released from storage proteins such as ferritin, which results in generation of the highly toxic hydroxyl radical by an iron catalyzed Fenton reaction. Therefore, the balance between ferritin and iron released from heme is important for protection of the cells against toxic free iron [Figure 4]. [31]
Figure 4: The relationship between ROS, iron, and HO-1 in psoriasis.

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c. Role of Nitric oxide

Nitric oxide (NO) is the next important intrinsic factor involved in the pathogenesis of psoriasis linked to ROS formation and induction of HO-1 expression. Keratinocytes constitutively express the neuronal isoform of NO synthase (NOS-1). Under inflammatory skin conditions (psoriasis), virtually all skin cells appear to be capable of expressing the inducible NOS isoform (iNOS). Low concentrations of NO trigger cell proliferation, whereas high concentrations are cytostatic. NO, released from keratinocytes at high concentrations, is considered to be a key inhibitor of cellular proliferation. As psoriatic keratinocytes express iNOS, potentially capable of high-output NO synthesis, one possible hypothesis for explaining the keratinocyte hyperproliferation is that iNOS activity in psoriasis lesions is too low to deliver anti-proliferative NO concentration.

An overexpression of a cytokine-induced cytosolic enzyme ARG1 (arginase 1) is seen in psoriasis lesions. The iNOS and ARG1 has an antagonistic interaction in psoriatic keratinocytes, which is mechanistically stimulating; this is because the balance between both enzymes is normally reciprocally regulated by Th1 and Th2 lymphocytes. Th1 cytokines induce iNOS and downregulate ARG1 expression. Thus, in psoriasis, the co-expression of iNOS and ARG1 represents an aberrant regulation of Th1 response. Moreover, it has been demonstrated that HO pathway is involved in keratinocyte proliferation mediated by NO. [31]

This strongly indicates an aberrant balance between ROS, NO generation, and HO-1 activity resulting in perpetuating abnormal proliferation of keratinocytes and chronic inflammatory status in the skin.


Treatment options include emollients and keratolytic agents, anthralin, tars, topical corticosteroids, vitamin D3 analogues, retinoids, methotrexate, cyclosporine, tacrolimus, and psoralens plus phototherapy. In general, topical treatment is begun first for mild to moderate psoriasis. A more aggressive initial approach may be indicated for severe psoriasis. Psoralen plus ultraviolet A (PUVA), the combination of ultraviolet light and drugs, is one of the most common photo chemotherapeutic regimens for psoriasis.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1]


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