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REVIEW ARTICLE
Year : 2017  |  Volume : 18  |  Issue : 1  |  Page : 1-8

Recent understanding of the etiopathogenesis of psoriasis


Department of Dermatology, KPC Medical College, Kolkata, West Bengal, India

Date of Web Publication12-Dec-2016

Correspondence Address:
Saumya Panda
Department of Dermatology, KPC Medical College, Kolkata, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2319-7250.195569

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  Abstract 


Psoriasis is a common inflammatory disorder of the skin. Although a lot is known regarding its pathogenesis, much remains to be elucidated and understood. Psoriasis is a disease of multifactorial origin where certain environmental factors acting on individuals with specific genetic predisposition leads to an immune dysregulation. Till now no single genetic or environmental entity has been found to be consistently associated with all cases of psoriasis. Hence, psoriasis has been considered by some to be a heterogeneous group of disorders where several disparate pathological processes result in a similar outcome. There is a huge array of potential genes now implicated and an equally large array of molecules (chemokines, cytokines, inflammatory mediators, signal transduction molecules, and transcription factors) found to be involved. Although new therapeutic options have opened up as a result, our inability to solve the puzzle and thoroughly understand the disease prevents their optimal utilization.

Keywords: Cytokines, etiopathogenesis, psoriasis


How to cite this article:
Ghosh A, Panda S. Recent understanding of the etiopathogenesis of psoriasis. Indian J Paediatr Dermatol 2017;18:1-8

How to cite this URL:
Ghosh A, Panda S. Recent understanding of the etiopathogenesis of psoriasis. Indian J Paediatr Dermatol [serial online] 2017 [cited 2019 Aug 23];18:1-8. Available from: http://www.ijpd.in/text.asp?2017/18/1/1/195569




  Introduction Top


Psoriasis is a common inflammatory disorder of the skin, yet it still remains an enigma. Although a lot is known regarding its pathogenesis, much remains to be elucidated and understood. This review aims to discuss the current concepts regarding the pathogenesis of the disease with possible therapeutic implications.

Psoriasis is a disease of multifactorial origin where certain environmental factors acting on individuals with specific genetic predisposition leads to an immune dysregulation and abnormal keratinization which results in the appearance of typical cutaneous lesions. However, till now no single genetic or environmental entity has been found to be consistently associated with all cases of psoriasis. Hence, psoriasis has been considered by some to be a heterogeneous group of disorders where several disparate pathological processes result in a similar outcome or cutaneous response.

Early-onset psoriasis and late-onset psoriasis are known to be different with respect to the genes implicated and the clinical behavior.[1],[2] This, however, may be an oversimplification. Certain researchers have divided the disease into six different clinical phenotypes on the basis of statistical clustering of clinical symptoms [Table 1].[3] Such a scenario may have significant consequences on our understanding of the disease and tailoring of therapeutic interventions to individual cases. However, it is worth noting that the French study is yet to be replicated in the non-Francophone parts of the world.
Table 1: Proposed clinical phenotypes of psoriasis

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  Immunology and Environmental Factors in Pathogenesis of Psoriasis Top


The environment and body's immunity (innate and adaptive) directed against it are closely knit and cannot be discussed in separation. Hence, in this section, both these factors have been discussed together as far as is practicable.

Physical trauma, psychological stress, certain drugs, infections (Streptococcus, Malassezia, Candida, Staphylococcus), metabolic syndrome, and dry weather conditions causing stress on the skin barrier can all precipitate or aggravate the disease by indirectly affecting the internal immunological balance.[4]

Psoriatic plaques are characterized by the following:

  • Dysregulation of proliferation and maturation of keratinocytes leading to acanthosis, hypogranulosis, and parakeratosis
  • Proliferation of dermal blood vessels, and
  • Infiltration of the skin by inflammatory cells.


Among these, it is difficult to understand which one is a primary or initial event serving as a trigger for subsequent processes and which one is a change secondary to the inflammatory process.

The interplay of different cells such as keratinocytes, dendritic cells, endothelial cells, T-lymphocytes, monocytes, and polymorphonuclear cells along with various cytokines produced by them result in the cutaneous lesions of psoriasis and as such considering it only as a T-cell disorder is an oversimplification. However, T-cell mediated inflammation does play a pivotal role in the pathogenesis of psoriasis.[5],[6],[7]

The earlier concept of psoriasis being solely a T-helper (Th) 1 mediated disorder has been replaced by the concept of combined Th1 and Th17 mediated inflammatory disease.[5],[6] The recognition of this new subset of helper T-cells (Th17) and Th22 cells and their distinct sets of cytokines (interleukin [IL] 23, IL-22) has opened up research for newer specific drugs. Other types of cells associated with innate immunity such as γδT-cells, natural killer (NK) cells, and NK-T cells may also have a role to play.[5] Decreased suppressive activity of regulatory T-cells (T-regs) seen in psoriatic lesions possibly leads to uncontrolled action of the other effector cells.[6] Hence, psoriasis is more aptly considered as the outcome of complex interactions within various subsets of T-cells instead of being a disease caused by a single subset.

These T-cells are possibly activated by antigens presented by the dendritic cells of the skin (namely Langerhans cells, dermal dendritic cells, myeloid, and plasmacytoid dendritic cells). However, the exact nature of the antigen still remains a matter of conjecture. The streptococcal M protein bears a structural similarity with the Type 1 keratins and may thus stimulate an immune reaction which can then cross react with specific tissue antigens in the skin, a concept known as molecular mimicry.[8] Keratin 17, ezrin, maspin, peroxiredoxin 2, and heat shock protein 27 are certain potential autoantigens which have sequences homologous to streptococcal proteins.[9] Such mechanisms possibly play an important role in patients with psoriasis who carry the human leukocyte antigen (HLA)-Cw6 allele. However, in other cases of psoriasis, the relationship is not as clear. Recognition of streptococcal peptidoglycan through pattern recognition receptors such as Toll-like receptor 2, and PG recognition proteins 1–4 is another mechanism of psoriasis induction due to altered immune response.[5],[10] These molecular mechanisms possibly underlie the beneficial effects of tonsillectomy in some cases of psoriasis which show aggravation after episodes of streptococcal infections.[11],[12]

The other immune cells such as macrophages produce tumor necrosis factor (TNF)-α, proteases, growth factors, and vascular endothelial growth factor (VEGF), which in turn perpetuate the inflammatory process and promote angiogenesis.[13] Mast cells similarly produce large quantities of TNF-α, interferon (IFN)-γ, IL-8, and VEGF causing recruitment of T-cells and neutrophils at inflammation site.[6]

Neutrophil activation appears to be important, especially in early and active psoriatic lesions though its role has not been clearly elucidated. Activated neutrophils degranulate to release a large amount of cytokines, proteases and elastases, cationic proteins (lactoferrin, etc.,), and play an important role in recruitment and activation of T-cells to the lesional site.[6],[7]

Keratinocyte proliferation and defective maturation are the hallmarks of psoriasis. The cytokines and other inflammatory mediators produced by the T-cells, dendritic cells, neutrophils, and macrophages activates the keratinocytes which increase their proliferation and they in turn produce various cytokines and growth factors to maintain and increase the inflammatory reaction and endothelial proliferation.[13] A primary epidermal barrier defect has been reported in uninvolved skin in psoriatics.[14] Whether this has any contribution in the pathogenesis of the disease is still a matter of conjecture.

The association of psoriasis with metabolic syndrome and the observation that patients with higher body mass index (BMI) often have a more severe disease points to the role of adipokines in the pathogenesis of psoriasis. Levels of certain adipokines in the serum have been found to increase the levels of Th17-related cytokines.[15] Serum resistin levels show a positive correlation with serum TNF-α and may be a potential marker for prognosis in patients with psoriasis.[16] Serum leptin and adiponectin levels have been found to be related with increased levels of IL-6 and IL-22, respectively.[15] This might explain the fact that lifestyle changes in the form of weight reduction, dietary modification, etc., have shown to benefit patients with psoriasis and increase the effectiveness of therapy.[17],[18],[19]

The inflammatory process involves interaction among a large number of cells of the immune system, keratinocytes, and endothelial cells and this process is mediated by a host of cytokines [Figure 1]. Although TNF-α, IFN-γ, and IL-23 appear to be the most important cytokines, numerous other cytokines and chemokines are also involved leading to an extremely intricate system of cell-to-cell communication, activation, and/or inhibition.[6] The various chemokines and inflammatory mediators and growth factors mediate their effects through various signal transduction molecules, transcription factors, etc., for example, Janus Kinase-signal transducers and activators of transcription pathways, and protein kinases. These various mediators along with related therapeutic molecules have been enumerated in [Table 2].
Figure 1: The interplay of innate and adaptive immunity in psoriasis

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Table 2: Cytokines, chemokines, and signaling molecules operating in psoriasis and their specific inhibitors

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  Genotypes of Psoriasis Top


There is a definite role of genetic factors in susceptibility and expression of the disease. This is supported by the increased incidence of psoriasis in relatives of index cases, and almost a three-fold increased chance of the disease in monozygotic twins compared to dizygotic ones.[36]

For a complex disease like psoriasis, a large number of genes may be implicated which may alone or in combination under the influence of certain environmental factors which cause the disease.

Multiple genes have been implicated of which genes coding for the HLA proteins are the most plausible candidates.[37] Other potential loci which affect other inflammatory pathways such as genes for IL-23 receptor subunit, endoplasmic reticulum amino peptidase-1, nuclear factor κB signaling, and cluster of DEFB genes coding for β-defensins may also have a role to play.[4] Mutations in genes coding for certain proteins expressed in the keratinocytes, for example, late cornified envelope protein 3B and 3C, corneodesmosin (CDSN), gap junction protein β2, and connexin 26 may impair proper barrier function of the skin with a resultant predisposition to the disease.[4],[38]

The important genes conferring susceptibility to psoriasis as found by linkage analyses are PSORS1 on 6p21.3, PSORS2 on 17q, PSORS3 on 4q, PSORS4 on 1cenq21, PSORS5 on 3q21, PSORS6 on 19p, PSORS7 on 1p, and PSORS9 on 4q31.[38]

Psors1 (6p21.3) is the locus most consistently associated with psoriasis. Very close to this locus lies the CDSN gene which is expressed in differentiated keratinocyte and its product plays an important role in cell-to-cell adhesion.[39] Mutations in this region may cause epidermal barrier dysfunction and predispose to the disease. The 6p region of the human genome also has the major histocompatibility complex class I genes among which the HLA-B13, HLA-B17, HLA-B57, HLA-A01, and HLA-Cw6 alleles appear to be consistently associated with the disease.[38] HLA-Cw*0602 is strongly associated with severe early-onset psoriasis and cases of guttate psoriasis.[40],[41] Bw 16 appears to be associated with early-onset disease, while B 27 with late-onset disease and psoriatic sacroiliitis. Bw 38 predisposes to psoriasis and distal arthritis, while B13 is associated with milder, more reversible disease.[42]

PSORS 2 locus on chromosome 17q has also been reported to promote susceptibility to psoriasis. However, for most of the other loci, the evidence is doubtful.[37]

Genetic variations in CX3CL1 (fractalkine) and/or CX3CR1 (receptor) may possibly enhance susceptibility to psoriasis as their products play an important role in chemotaxis, migration, and extravasation of NK cells, T-lymphocytes, monocytes and other immunocompetent cells.[43] These genes seem to be associated with other systemic inflammatory disorders such as rheumatoid arthritis and cardiovascular diseases, and their expression appears to be elevated in psoriatic plaques.[44],[45]

The role of polymorphisms in the cytotoxic T-lymphocyte antigen-4 (CTLA-4) methylene tetrahydrofolate reductase, IL-1β, and IL-1 receptor antagonist genes has been suspected, but their association has not been proven.[46],[47],[48],[49]

TNF-α gene is another potential candidate gene promoting susceptibility and predicting treatment response to anti-TNF therapy in psoriasis. TNFα-308 G/A polymorphism seems to have a potential association with disease causation but no association with histological severity of the disease.[50]

TNF receptor superfamily (TNFRSF) 1B T allele carriers show a better response to anti-TNF therapy, while individuals carrying TNFRSF1A allele has no relationship with the response to anti-TNF therapy.[51]

A candidate gene that has attracted a lot of attention in recent times is the caspase recruitment domain family, member 14 (CARD 14) CARD 14 gene. Much of the attraction of the researchers for this genetic pathway is due to the fact that mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) inhibitors might be therapeutically beneficial for psoriasis patients with CARD 14 mutations. Whether MALT1 inhibitors may also be useful for the treatment of more common forms of psoriasis is currently under investigation.[52]


  Childhood Psoriasis Top


Childhood or early-onset psoriasis as compared to the late-onset variety shows a higher percentage of positive family history and a relatively higher predominance of HLA-Cw6 allele but usually no difference in clinical severity of disease.[53] Environmental exposure to tobacco, obesity/raised BMI, and stressful life events are the risk factors for development or aggravation of the disease.[54],[55] However, exclusive breastfeeding, introduction of cow milk in the 1st year of life, and prematurity at birth does not appear to have any influence.[54] Although plaque type of psoriasis is the most common clinical variant in many cases, it is preceded by the eruption of guttate lesions.[56] Preceding streptococcal infection and raised antistreptolysin O (ASO) titer have been reported to be more common in cases of guttate psoriasis with eventual resolution as compared to cases with subsequent progression to plaque type of disease.[57] Hence, ASO titer may have a predictive value regarding prognosis. Psoriasis and atopic dermatitis share several common genetic susceptibility loci such as 1q21, 3q21, 17q25, and 20p and in childhood, these two diseases may be difficult to differentiate and in many cases may coexist.[58]


  Conclusion Top


Ongoing research regarding psoriasis has left us with a problem of plenty. There is a huge array of potential genes implicated and an equally large array of molecules (chemokines, cytokines, inflammatory mediators, signal transduction molecules, and transcription factors) involved. Although new therapeutic options have opened up as a result, our inability to solve the puzzle and thoroughly understand the disease prevents their optimal utilization. Hopefully, with increasing research, as the situation becomes clearer, it will be possible to provide more effective and individualized treatment to patients of psoriasis.

Financial Support and Sponsorship

Nil.

Conflicts of Interest

There are no conflicts of interest.

 
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    Tables

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