Etiopathogenesis Of Psoriasis Research Articles

Plexin B2 tissue expression and related gene polymorphisms in psoriasis and their relation to NB-UVB and Acitretin therapy

Psoriasis is a chronic, immune-mediated, hyperproliferative skin disease. Etiopathogenesis of psoriasis is not well understood. Plexin B2 was found to have effects on CD100-mediated T-cell morphology and expressed in the immune system. It may play a role in the pathogenesis of psoriasis. To assess the tissue level of plexin-B2 and plexin B2 related gene polymorphism which is signal regulatory protein gamma (SIRPγ-rs71212732) in psoriatic patients before and after NB-UVB, acitretin therapy alone or in combination and to detect correlation between level of tissue plexin B2 and disease severity and improvement. This single blinded randomized controlled trial was carried on 50 psoriatic patients and 50 healthy controls. Psoriasis Area and Severity Index score (PASI) was used to evaluate the disease severity. Tissue plexin-b2 level was measured using ELISA and SIRPγ-rs71212732 (T\\C) was assessed using TaqMan™ assays and real-time PCR. A significant lower tissue plexin-B2 level was observed in control group (2.9 ± 0.6 pg/g) than cases (25.8 ± 2.8, pg/g) (p < 0.001). Also, a significantly higher tissue plexin-B2 level was observed in sever psoriasis (32.7 ± 3.8 pg/ml) in than moderate psoriasis (13.6 ± 2.1 pg/ml, p = 0.001). Tissue plexin B2 was positively correlated with diseases severity. Significantly higher (TC& TT) genotypes and mutant (C) allele among patients compared to the controls, p < 0.001 for all. Tissue plexin-b2 level was high in psoriasis vulgaris with positive correlation with disease severity and decreased after treatment. This may indicate a role of plexin-b2 in psoriasis vulgaris pathogenesis.

Assessment of NADH/NAD+ Redox Imbalance in Psoriatic Lesions Using the FMSF Technique: Therapeutic Aspects.

Mitochondrial dysfunction has been linked to psoriasis, and it may be an important underlying factor contributing to this disease. However, a precise methodology for assessing mitochondrial dysfunction has yet to be developed. One promising approach is to measure NADH autofluorescence from the affected skin areas. In this study, we show that Flow-Mediated Skin Fluorescence (FMSF) can be used for the non-invasive assessment of mitochondrial dysfunction in psoriasis. The fluorescence level at baseline and the half-time of ischemic growth (t1/2) derived from the FMSF traces can be used for the non-invasive assessment of NADH/NAD+ redox imbalance in psoriatic lesions compared to unaffected skin. These results are supported by an analysis of the key FMSF parameters: Reactive Hyperemia Response (RHR) and Hypoxia Sensitivity (HS). This method not only contributes to understanding the biochemical processes involved in the etiopathogenesis of psoriasis, but it also provides a basis for identifying new drug targets and improving the treatment process.

Genetics of Generalized Pustular Psoriasis: Current Understanding and Implications for Future Therapeutics.

Psoriasis is a chronic inflammatory skin disease characterized by the appearance of clearly demarcated erythematous and scaly plaques. It can be divided into various types, including plaque, nail, guttate, inverse, and pustular psoriasis. Plaque psoriasis is the most commonly occurring type, though there is another rare but severe pustular autoinflammatory skin disease called generalized pustular psoriasis (GPP), which manifests with acute episodes of pustulation and systemic symptoms. Though the etiopathogenesis of psoriasis is not yet fully understood, a growing body of literature has demonstrated that both genetic and environmental factors play a role. The discovery of genetic mutations associated with GPP has shed light on our comprehension of the mechanisms of the disease, promoting the development of targeted therapies. This review will summarize genetic determinants as known and provide an update on the current and potential treatments for GPP. The pathogenesis and clinical presentation of the disease are also included for a comprehensive discussion.

Clinical case: switching from basic therapy with methotrexate to therapy with netakimab, an IL-17 inhibitor, in a patient with severe psoriasis

Currently, psoriasis occupies a leading position in the structure of chronic recurrent dermatological diseases. The modern view on the etiopathogenesis of psoriasis allows us to consider this disease as a systemic, genetically determined, immune-mediated process, which manifests itself not only in the form of damage to the skin, but also leads to the development of various comorbid conditions (lesion of the musculoskeletal system, cardiovascular system, excretory system , metabolic disorders, etc.). This fact radically changes the approach to the treatment of patients with psoriasis, to the selection of a systemic drug. The main points in the management of patients with psoriasis, especially of moderate and severe course: interdisciplinary examination of the patient, prevention of the development of comorbid conditions and irreversible (sometimes disabling) changes in internal organs and systems, timely administration of systemic therapy. The article presents modern aspects of the etiopathogenesis of psoriatic disease, the advantages of genetically engineered biological therapy, and a clinical case of treating a patient with severe psoriasis. A 48-old-patient E. who had been suffering from extensive psoriasis vulgaris for 16 years, which manifested after pregnancy and childbirth, was proscribed the systemic therapy. In July 2022, the patient reported oedema that developed in the lower extremities and face while taking methotrexate, and was examined by a nephrologist. Microalbuminuria nephropathy was diagnosed, which served as a reason for adjusting the systemic therapy for psoriasis. The patient had to be switched to the genetically engineered biological therapy. After 3 subcutaneous injections of netakimab at a dose of 120 mg/week, psoriasis went into a steady-state showing the trend towards a regressing stage. The psoriasis severity index scores decreased by the end of the initiating course of therapy.

Dietary inflammatory potential and psoriasis: A cross-sectional study.

Diet is an important source of inflammation, and diet-induced inflammation might be associated with the etiopathogenesis of psoriasis. This study aimed to explore the relationship between dietary inflammatory index (DII), a literature-derived dietary tool to measure individual dietary inflammatory potential, and incident psoriasis. This was a cross-sectional study based on the 2003-2006 and 2009-2014 National Health and Nutrition Examination Surveys. The calculation of DII was based on 24-h dietary recall. Psoriasis was defined by a self-reported medical questionnaire. Logistic regressions were introduced to calculate the odds ratio (OR) and 95% confidence interval (CI) of psoriasis relative to DII. Restricted cubic splines (RCS) were used to test the nonlinear relationship in the regression model. A total of 13 284 participants with an average age of 48.94 ± 17.71 years were enrolled. The prevalence rate psoriasis was 2.88% (95% CI 2.61, 3.18). Incident psoriasis was not associated with DII in a multivariable logistic regression model (OR=1.00, 95% CI 0.89, 1.11). Compared to participants in the lowest DII tertile, OR for those in the highest was 0.81 (95% CI 0.51, 1.28, P for trend=0.0974). Subgroup analysis indicated that DII was still not associated with psoriasis in participants with different population settings. RCS showed that DII was not associated with psoriasis in either an overall or a nonlinear manner. Although a proinflammatory diet could lead to several health risks, psoriasis occurrence might not be associated with dietary inflammatory potential in this cross-sectional study.

Psoriasis and COVID 19: Exacerbation Following Hydroxychloroquine: A Case Report

Psoriasis is a chronic and multisystemic inflammatory disease, several factors can trigger it or aggravate it, including certain drugs including hydroxychloroquine. This drug, widely prescribed for COVID 19 infection, can trigger a flare-up of psoriasis, particularly the pustular form. Furthermore, patients with coronavirus 2019 infection, have increased plasma concentrations of inflammation-related cytokines which are also implicated in the etiopathogenesis of psoriasis, this may suggest that COVID-19 may be a new entity which exacerbates psoriasis. We report the observation of a patient who presented with psoriasis exacerbated by taking hydroxychloroquine following infection with covid 19.

Types of Psoriasis and Their Effects on the Immune System.

Psoriasis is a chronic inflammatory skin disease which is identified by the appearance of erythematous that is clearly demarcated, scaly plaques. It is a skin disease seen regularly around the elbow, scalp, trunk, and also on the knees. Psoriasis is a commonly occurring chronic disease with no cure. In psoriasis, which is thought to be an immune system-related problem, the cells of the skin grow quicker than normal cells. The rapid turnover of cells is responsible for the dry scaly patches seen clinically, also called plaque type of psoriasis. The etiopathogenesis of psoriasis is not yet fully understood. It is considered an outcome of some alteration of the cells in the immune system, which fights infections, but here, it attacks healthy cells, which is the problem. Researchers believe both environmental and genetic factors play a role. It is commonly known that psoriasis is not contagious as it does not spread by air or water. There is a chance of increasing the risk of acquiring psoriasis, also worsening the disease severity by smoking and tobacco consumption. Anyone irrespective of age or gender can develop psoriasis. Psoriasis is divided into various kinds: plaque, nail type, guttate, or inverse, also pustular. The most commonly occurring type of psoriasis is plaque psoriasis, seen with itchy, dry, scales covering patches of skin that are raised.

Etiopathogenesis of Psoriasis from Genetic Perspective: An updated Review.

Psoriasis is an organ-specific autoimmune disease characterized by the aberrant proliferation and differentiation of keratinocytes, leading to skin lesions. Abnormal immune responses mediated by T cells and dendritic cells and increased production of inflammatory cytokines have been suggested as underlying mechanisms in the pathogenesis of psoriasis. Emerging evidence suggests that there is a heritable basis for psoriatic disorders. Moreover, numerous gene variations have been associated with the disease risk, particularly those in innate and adaptive immune responses and antigen presentation pathways. Herein, this article discusses the genetic implications of psoriatic diseases' etiopathogenesis to develop novel investigative and management options.

Psoriasis: An Immunogenetic Perspective.

Psoriasis is an erythematous-squamous dermatosis with a polygenic inheritance history. Both environmental and genetic factors play a role in the etiology of the disease. Over the past two decades, numerous linkage analyzes and genome-wide association studies have been conducted to investigate the role of genetic variation in disease pathogenesis and progression. To date, >70 psoriasis susceptibility loci have been identified, including HLA-Cw6, IL12B, IL23R, and LCE3B/3C. Some genetic markers are used in clinical diagnosis, prognosis, treatment, and personalized new drug development that can further explain the pathogenesis of psoriasis. This review summarizes the immunological mechanisms involved in the etiopathogenesis of psoriasis and recent advances in susceptibility genes and highlights new potential targets for therapeutic intervention.

Novel Therapeutic Target(s) for Psoriatic Disease.

Psoriasis and psoriatic arthritis, together known as psoriatic disease, is highly prevalent chronic relapsing inflammatory disease affecting skin, joints or both and is associated with several comorbidities such as cardiovascular, metabolic, psychiatric, renal disease etc. The etiopathogenesis of psoriasis is complex and mainly driven by aberrant immune response owing to the genetic susceptibility and various environmental factors such as trauma, infections and drugs. Recent advances in understanding molecular and cellular pathways have identified tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), IL-23, IL-22 as major contributors in psoriasis pathogenesis. Advances in the knowledge of pathophysiology, the interaction of autoinflammation and clinical phenotypes have led to the development of highly effective targeted therapeutic agents which include TNF-α, IL-17, IL-23, IL-1 α/β or IL-36 inhibitors or receptor blockers, small molecule drugs like phosphodiesterase-4 inhibitors (apremilast), Janus kinase (JAK) inhibitors, retinoic acid receptor-related orphan receptor γt (RORγt) inhibitors. These novel drugs have promised the potential of improved disease control. In recent years, the transition from biologics to biosimilars especially with TNF-α inhibitors had significant impact on decreasing health care cost and increasing therapeutic options to the patients. However, selection of right treatment for an individual patient still remains challenging. Moreover, interplay between different epigenetic mechanisms such as the DNA methylation, chromatin modifications and noncoding RNA regulation has recently been started to be deciphered. Enzymes inhibitors involved in epigenetic pathways such as DNA methyltransferases and histone deacetylases demonstrated to restore normal epigenetic patterns in clinical settings and have provided the potential as novel therapeutic targets for psoriasis. In this review, we will discuss novel biologic agents and newer therapeutic approaches in treatment of psoriatic disease.

Update on the etiopathogenesis of psoriasis (Review).

Psoriasis is one of the most common immune-mediated chronic inflammatory skin disorders, involving hyperproliferative keratinocytes and infiltration of T cells, dendritic cells, macrophages, and neutrophils. Multiple factors appear to play important roles in the pathogenesis of psoriasis. These environmental (e.g., infectious agents and trauma), genetic, and immunologic factors are reviewed in this article. Although the pathogenesis of psoriasis remains to be established, data suggesting immune cell dysregulation in the skin are available. The involvement of the immune system, particularly T cells, in the etiopathogenesis of psoriasis is discussed in this review, indicating a potential justification for innovative treatment intervention. Besides describing pathogenic T cells, the aim of the review was to assess the function of newly identified antimicrobial peptides (AMPs), interleukin (IL)-23, IL-17, and tissue resident memory cells (TRMs), and their role in psoriasis. Furthermore, new insights were presented regarding TRMs, a recently identified subset of memory T cells, and the role they play in the local memory of disease, making them a potential new therapeutic target in psoriasis. Finally, current developments in T-cell research and cytokine-targeted therapy for psoriasis treatment are reviewed.

Korelasi Kadar Serum &lt;i&gt;Nitric Oxide&lt;/i&gt; (NO) dengan Tipe dan Derajat Keparahan Psoriasis

Psoriasis is a chronic, immune-mediated disorder that results from a polygenic predisposition. Nitric oxide (NO) has been considered as important factors in the pathogenesis of psoriasis. This study aims to determine the correlation of serum NO levels with the type and severity of psoriasis. This cross-sectional study was conducted from May to September 2018. Difference in the average of serum NO levels in psoriasis patients with control groups is analyzed using t-test. The Spearman correlation test was used to see the correlation of serum NO levels with type and severity of psoriasis measured by Psoriasis Area and Severity Index (PASI) score. There was significant difference between serum NO level in the control group compared to the group of psoriasis patients (p=0.037). Patient with generalized pustular psoriasis has the highest mean of NO level (59.07 µmol/L). There was no significant correlation between serum NO level with type (r=0.008, p=0.9710 and severity (r=0.157, p=0.486) of psoriasis. Nitric oxide levels are elevated in psoriasis patients, which indicate that oxidative stress plays an important role in the etiopathogenesis of psoriasis.

Frequency, Distribution and Genotyping of Malassezia Species in Patients with Psoriasis vulgaris

Abstract Background: Malassezia species are reported to play a role in the etiology of Psoriasis vulgaris. Objective: The aim of this study was to determine the presence, frequency, distribution, and genotyping of skin colonization of Malassezia species in Psoriasis vulgaris and to compare with healthy individuals and to investigate its relationship with the severity of the disease. Methods: Skin samples were taken from scalp, arm, body, and leg of 34 psoriasis patients (lesional/non-lesional skin) and 30 healthy volunteers. Overall, 392 skin scraping samples were taken for the isolation of Malassezia species, which were incubated on the modified-Dixon agar. Conventional culture methods were used for Malassezia species identification. In isolates, genotyping was carried out by PCR-RFLP method. Results: In the samples from psoriatic lesions, most frequently isolated Malassezia species were M.globosa and M.furfur. Similarly, the most frequently isolated species in healthy volunteers was M. globosa; followed by M.restricta and M.sympodialis. The M.furfur isolation rate in psoriatic scalp and leg lesions of the patients was significantly higher than in healthy volunteers. There was no relationship between the severity of the disease and the isolated species. Conclusion: It was found that there was a difference between patients with psoriasis and healthy controls regarding presence and frequency of Malassezia species. Therefore, our study results support the view that Malessezia species may be associated with the etiopathogenesis of psoriasis. In addition, we surmise that the treatment applications for the regulation of skin microbiota of psoriasis patients will contribute positively to the treatment of psoriasis.

Role of resolvin D1 in psoriasis before and after narrowband ultraviolet B phototherapy: A case-control study.

Resolvin D1 (RvD1) is an endogenous lipid mediator that originated from docosahexaenoic acid that stimulates a bimodal mechanism in the anti-inflammatory activity in addition to regulation of the inflammatory reaction. The study aimed at assessing the tissue level of RvD1 in psoriasis to study its role in the etiopathogenesis of psoriasis, studying the action of NB-UVB on the level of resolvin D1 in psoriasis, and raising the possibility of using resolvin D1 as a new therapy for psoriasis in the future. This case-control study included 20 psoriasis patients and 20 healthy controls. Patients took narrowband ultraviolet B (NB-UVB) for 36 sessions. Skin biopsies were taken before and after treatment from patients and from controls to assess the expression of RvD1 by a quantitative real-time polymerase chain reaction. Our findings revealed a statistically significant difference (P < .001) between psoriasis patients (either before or after treatment) and controls with lower levels of RvD1 in psoriasis patients. On comparing the RvD1 levels in psoriasis patients before and after treatment, a statistically significant increase was detected after treatment (P < .001). Tissue RvD1 levels in psoriasis patients were lower than healthy controls and increased after NB-UVB treatment in psoriasis patients. Thus, it is suggested that RvD1 might have a role in the etiopathogenesis of psoriasis. Moreover, the significantly up-regulated tissue levels of RvD1 in patients after treatment with NB-UVB highlighted a novel mechanism of phototherapy-mediated response in psoriasis by up-regulating RvD1 level.

Is prenatal testosterone-estrogen balance associated with psoriasis?

The etiopathogenesis of psoriasis is not understood; however, psoriasis is affected by hormones, particularly the sex steroids. The second-to-fourth digit (2D:4D) ratio, which is an indicator of prenatal sex hormone balance, has been studied in various diseases that are affected by hormones. A total of 369 individuals comprising 172 patients with psoriasis and 197 healthy volunteers were included in the study. Patients with psoriasis were divided into type-1 and type-2, according to age of onset and family history. The 2D:4D ratio of both hands was recorded for all participants. Females in the psoriasis group had a lower 2D:4D ratio in both hands compared with those in the control group, with no significant difference. Males in the psoriasis group had a higher 2D:4D ratio for both hands compared with those in the control group (P = .009 and P < .001 for the right and left hands, respectively). Further, male patients with type-1 psoriasis had a lower 2D:4D ratio compared to those with type-2 psoriasis. Our results suggest that an alteration of the estrogen-testosterone balance due to prenatal testosterone activity is an independent predisposing factor for psoriasis in males.

Avaliação dos hormônios sexuais e da prolactina em pacientes portadores de psoríase em placa atendidos em serviço de referência do estado do Pará

Objetivo: Avaliar os níveis circulantes dos hormônios sexuais e da prolactina em pacientes com psoríase em comparação com controles saudáveis e determinar a correlação entre os níveis desses hormônios e a gravidade da doença. Métodos: Os níveis de estrogênio, progesterona, testosterona, hormônio folículo estimulante (FSH), hormônio luteinizante (LH) e prolactina (PRL) foram medidos em 40 pacientes com psoríase e 20 controles saudáveis. Resultados: Observou-se que os pacientes com psoríase apresentaram maiores níveis séricos de FSH e LH e menores de testosterona e estrogênio em relação aos controles saudáveis, embora essa diferença não tenha sido estatisticamente significativa. Não houve diferenças nos níveis de progesterona entre os 2 grupos avaliados. No entanto, os níveis séricos de prolactina foram significativamente maiores entre os pacientes com psoríase quando comparado aos controles saudáveis. Além disso, uma correlação positiva estatisticamente significante foi encontrada entre a prolactina e o PASI (Índice de gravidade da psoríase por área). Conclusão: Nesse sentido, infere-se que a prolactina possa desempenhar um papel na etiopatogenia da psoríase. No entanto, estudos de seguimento a longo prazo são necessários para validar a importância dessas associações.

Thiol/disulphide balance in patients with psoriasis.

IntroductionPsoriasis is a common chronic inflammatory skin disease with unknown etiopathogenesis.AimTo examine the thiol/disulfide balance in psoriasis patients and to compare the results with a healthy control group.Material and methodsEighty patients with psoriasis and 80 healthy individuals who were age- and gender-matched with these patients were included in this study. Serum native thiol, disulfide and total thiol levels were measured by a new automated method developed by Erel and Neselioglu. Disulphide/total thiol, disulphide/native thiol and native thiol/total thiol were calculated.ResultsWhile there was no statistically significant difference in terms of disulphide levels (SS) between the patient and control groups (p > 0.05), there were significant differences in terms of total thiol and native thiol (SH) levels, SS/SH, SS/total thiol and SH/total thiol ratios between the patient and control groups (p < 0.05). There was a statistically significant relationship between duration of the disease and the disulfide/native thiol ratio (p > 0.05).ConclusionsIn recent years, there have been few studies on the role of oxidative stress in the etiopathogenesis of psoriasis. In this study, we investigated in psoriasis patients, thiol/disulfide balance as a new oxidative stress marker. The results were compared with a healthy control group. Our results showed that thiol/disulphide balance shifted towards disulphide in psoriasis patients. This is important as a finding that supports the role of oxidative stress in the pathogenesis of psoriasis.

Risankizumab in the treatment of psoriasis - literature review.

Risankizumab is a humanized, monoclonal antibody directed against subunit p19 of interleukin 23 (IL-23). In February 2019, risankizumab was approved for the treatment of moderate to severe psoriasis. The aim of the work is to collect up-to-date information on risankizumab and present its mechanism of action and recent clinical trials in which it was applied. This work also compares the mechanisms of action of risankizumab and ustekinumab and their importance in the treatment of psoriasis and describes the role of IL-23 in the etiopathogenesis of psoriasis. The work also refers to the effectiveness of risankizumab treatment and its safety profile. The results of molecular and histological studies that show changes in psoriatic skin after risankizumab treatment are also described.

SERUM PROLACTINE LEVEL IN PATIENTS OF PSORIASIS VULGARIS AND ITS CORRELATION WITH DISEASE SEVERITY: A CASE-CONTROL STUDY

Background: Psoriasis is an autoimmune chronic inflammatory disorder affecting the skin mediated by T-lymphocytes resulting in production of cytokines which cause hyperproliferation of keratinocytes. Several factors and hormones like Prolactin have an action similar to these cytokines in promoting the multiplication of keratinocytes and other cells like lymphocytes and epithelial cells may have a role on the etiopathogenesis of psoriasis.&#x0D; Aim:-The aim of study is to compare the serum Prolactin levels in patients of psoriasis with a control group.&#x0D; Setting and study design: This is a case-control study conducted in the department of Dermatology, Venereology and Leprosy GMC, Kota over a period of 1year from July 2017 to June 2018&#x0D; Material and method: The study included 100 cases of psoriasis (60 males and 40 females) and 100 controls similar for age and sex. Serum Prolactin levels were measured by ECLIA and results were obtained.&#x0D; Statistical analysis: Mean and standard deviation were calculated for each variable. Statistical significance of the results was analyzed using correlation analysis (Pearson correlation coefficient) and independent samples t-test.&#x0D; Statistical significance was assumed at p value&lt;0.05.&#x0D; Result: Serum Prolactin level was significantly higher in cases of psoriasis compared to controls (p-value &lt;0.001). PASI score and serum Prolactin levels were found to have a positive correlation (r value = 0.337; p-value: 0.001). No significant correlation was found between serum levels of Prolactin and duration of disease r value= -0.034, P value =0.733). Serum Prolactin level was higher in male patients compared to females patients.&#x0D; Conclusion:- High serum Prolactin may be a biological marker of disease severity in psoriasis and may have a role in the pathogenesis of psoriasis. Further studies with large sample size are required to confirm this hypothesis.

The role of GNLY gene polymorphisms in psoriasis pathogenesis

Background:Psoriasis is a systemic inflammatory disorder that involves complex pathogenic interactions between the innate and adaptive immune systems. The most accepted mechanism in the etiopathogenesis of psoriasis is the induction of inflammation with keratinocyte hyperproliferation. Granulysin (GNLY) is a cytolytic antimicrobial peptide (AMP) that is secreted together with granzyme and perforin from the granules of human cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. It has been immunohistochemically proven that the expression of granulysin is increased in lesions of psoriasis.Objective:This study aimed to investigate the relationship between psoriasis disease and granulysin gene polymorphisms.Methods:GNLY rs7908 and rs10180391 polymorphisms were studied by PCR-RFLP in 100 psoriasis patients under treatment in the Dermatology Polyclinic of Bulent Ecevit University. In addition, 100 healthy individuals with similar age and sex distribution were used as a control group.Results:In the control group, GNLY rs7908 CC genotype was significantly higher than in psoriasis patients (P= 0.031; OR= 0.305; Cl= 0.305 (0.121 - 0.773). In our study, the genotype distributions in patients and control groups were GNLY rs7908 (SNP) GG (51%, 37%), GC (41%, 44%), CC (8%, 19%); GNLY rs10180391 (SNP) from the CC (41%, 44%), CT (42%, % 41), TT (17%, 15%).Study limitations:The study only included Turkish patients.Conclusion:Our findings showed that GNLY rs7908 CC genotype and C allele had a protective effect against psoriasis and decreased the disease severity (according to PASI score), whereas rs10180391 SNP did not show any effective role in psoriasis pathogenesis.