Pathogenesis Of Psoriasis Vulgaris Research Articles

The Efficacy of Topical Formulation Containing Ciplukan (Physalis angulata Linn.) in Modulating Interleukin-17 and Interferon Gamma Expression in Mice (Mus musculus) Psoriasis Model.

Interleukin 17 (IL-17) and interferon gamma (IFN-γ) play a role in the pathogenesis of psoriasis vulgaris (PV). Topical corticosteroids are still utilised as first-line therapy for mild to moderate PV. However, long-term use of corticosteroid is associated with various side effects. Physalis angulata Linn. (Ciplukan) possesses anti-inflammatory properties that could serve as a potential alternative topical therapy for PV. To assess the efficacy of topical ciplukan as an anti-inflammatory agent targeting the expression of IL-17 and IFN-γ. Psoriasis was induced using imiquimod cream, therefore divided into five groups. Group I, the psoriasis control group, received only imiquimod cream. Groups C1 and C2 received imiquimod cream followed by a mixture of Ciplukan and vaseline in a 1:2 and 1:4 ratio, respectively. Group M, the standard therapy group, received imiquimod cream, followed by mometasone furoate cream. Lastly, group V, the vehicle group, received imiquimod cream followed by vaseline album. Expression of IL-17 and IFN-γ in mice's skin tissue was analysed using reverse transcription polymerase chain reaction (RT-PCR) after seven days of treatment. The mean expression of IL-17 in Group C1 (22.60) was significantly lower (p = 0.012) than in the psoriasis control group (23.60), and there was no significant difference (p = 0.613) in Group M (22.41). The mean expression of IFN-γ in Group C1 (26.97) and Group C2 (27.03) was also significantly lower (p = 0.026 and p = 0.026, respectively) than Group I (28.80), and there was no significant difference (p = 0.180 and p = 0.093, respectively) than Group M (26.03). Expression of IL-17 and IFN-γ in the ciplukan group is lower than in the psoriasis control group, and there is no significant difference compared to the standard therapy group.

Role of serum IL-26 in Pathogenesis of Psoriasis vulgaris

Role of serum IL-26 in Pathogenesis of Psoriasis vulgaris

Clinical Significance of Decreased TIPE2 Expression in Peripheral Blood Mononuclear Cells of Patients with Psoriasis Vulgaris

Psoriasis is an immune system disorder induced by the interaction of the polygenic background and environmental factors. Tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (TNFAIP8L2, TIPE2), a regulator of immunity, is differentially expressed in tumors, inflammation, and autoimmune diseases. However, to our knowledge, no study has evaluated TIPE2 expression in patients with psoriasis vulgaris. The present case-control study aimed to determine the expression levels of TIPE2 mRNA in the peripheral blood mononuclear cells (PBMCs) of patients with psoriasis vulgaris and analyze the correlation between TIPE2 and other inflammatory cytokine variations in the pathogenesis of psoriasis vulgaris. Thirty-three patients with psoriasis vulgaris and thirty-one healthy volunteers were enrolled from October 2021 to March 2022. The mRNA expression levels of TIPE2, RELA (NF-κb p65), TNF-α, IL-10, IL-6, and IL-1β in PBMCs were determined using qPCR. The severity of psoriasis vulgaris was determined according to the Psoriasis Area and Severity Index (PASI) scores. TIPE2 mRNA expression significantly decreased, while the expression of RELA, TNF-α, IL-10, IL-6, and IL-1β increased in patients with psoriasis vulgaris compared with that in the healthy control group. In addition, the expression levels of TIPE2, RELA, TNF-α, and IL-1β positively correlated with the PASI score. TIPE2 mRNA expression negatively correlated with IL-6 and positively correlated with TNF-α. Moreover, TIPE2 mRNA expression was higher in the active stage than that in the stationary stage. Notably, TNF-α expression levels were higher in patients with psoriasis vulgaris combined with a history of respiratory infection. TIPE2 may contribute to the pathogenesis of psoriasis and be a potential biomarker of psoriasis vulgaris.

The study of GSDMB in pathogenesis of psoriasis vulgaris.

Gasdermin (GSDM) B is a member of the GSDM family, which is a protein that may be involved in the cell pyroptosis process and is associated with inflammatory diseases. To explore the correlation between GSDMB and psoriasis vulgaris. Skin lesions from 33 patients with psoriasis vulgaris and 69 normal controls were collected. ELISA and Western blot were adopted to detect proteins. The HaCaT cell line was transfected with 3 sets of interfering sequence siRNA, and the mRNA and protein levels before and after the transfection were measured by qPCR and Western blot respectively, so as to establish a cell model with low GSDMB gene expression; the MTT method was used to detect cells viability, flow cytometry to detect cell apoptosis. The level of GSDMB protein in the skin lesions of patients with psoriasis vulgaris was lower than that in normal skin tissues (P < 0.05). The mRNA and protein expression levels of the target gene in the siRNA-GSDMB-3 group were lower than those in the control group (P < 0.05). The proliferation of HaCaT cells was decreased by MTT method and flow cytometry, and the apoptosis rate was increased (P < 0.05). The expression level of GSDMB in psoriasis vulgaris lesion tissue is lower than that of normal skin tissue. The down-regulation of GSDMB expression can inhibit cell proliferation and promote cell apoptosis. GSDMB may play a role in the pathogenesis of psoriasis by affecting the differentiation of keratinocytes and the function of T cells.

Possible Role of lncRNA MEG3-microRNA-21 and Endoplasmic Reticulum (ER) Stress Proteins in the Pathogenesis of Psoriasis Vulgaris.

Psoriasis is a chronic inflammatory immune mediated disease arising from interaction between genetic risk variants and the environment. Maternally expressed gene3 (MEG3) is a long noncoding RNA (lncRNA) known for gene transcription regulation and inhibiting proliferation. MEG3 competes with microRNA (miRNA-21) influencing cell proliferation and apoptosis balance. Endoplasmic reticulum (ER) stress proteins promote cell survival via unfolded protein response (UPR) influenced by MEG3. We aimed to detect the possible role of MEG3, miRNA-21 and ER stress proteins in pathogenesis of psoriasis vulgaris. Human GRP78, ATF6, caspase3 tissue levels were assayed by Enzyme Linked Immunosorbent Assay (ELISA). Assessment of long non-coding MEG3 and miRNA 21 expressions was done by quantitative real time polymerase chain reaction (qRT-PCR). Expression of MEG3 was significantly downregulated, while miRNA-21 was remarkably upregulated, ER stress proteins GRP78, ATF6, and caspase 3 all showed low levels in homogenized psoriatic lesions when compared to normal skin. miRNA 21 and MEG3 were identified as possible diagnostic markers for psoriasis vulgaris. MEG3 is barely expressed in psoriatic lesions while miRNA-21 expression is remarkably elevated but when correlated to each other there was unexpected positive correlation. MEG3 and miRNA-21 were identified as possible diagnostic markers for psoriasis. Undifferentiated psoriatic lesions have very weak UPR.

Reduction of Methyltransferase-like 3-Mediated RNA N6-Methyladenosine Exacerbates the Development of Psoriasis Vulgaris in Imiquimod-Induced Psoriasis-like Mouse Model.

N6-methyladenosine (m6A) methylation is the most pervasive and intensively studied mRNA modification, which regulates gene expression in different physiological processes, such as cell proliferation, differentiation, and inflammation. Studies of aberrant m6A in human diseases such as cancer, obesity, infertility, neuronal disorders, immune diseases, and inflammation are rapidly evolving. However, the regulatory mechanism and physiological significance of m6A methylation in psoriasis vulgaris are still poorly understood. In this study, we found that m6A methylation and Methyltransferase-like 3 (METTL3) were both downregulated in psoriatic skin lesions and were negatively correlated with Psoriasis Area and Severity Index (PASI) scores. Inhibiting m6A methylation by knocking down Mettl3 promoted the development of psoriasis and increased its severity in imiquimod-induced psoriasis-like model mice. Our results indicate a critical role of METTL3- mediated m6A methylation in the pathogenesis of psoriasis vulgaris.

833 Reintroduction of caveolin-1 scaffolding domain improves pathogenesis of psoriasiform dermatitis

Psoriasis is a chronic, inflammatory skin disease characterized by well-defined, erythematous plaques with silvery scale secondary to aberrant keratinocyte proliferation. We have previously identified that a structural membrane protein caveolin-1 (Cav1) is involved in regulation of aberrant keratinocyte proliferation and differentiation, and thus the aim of this study was to elucidate the role of Cav1 in pathogenesis of psoriasis vulgaris. We utilized spatial genomic & proteomic analyses combined with immunohistochemistry (IHC) with patient samples and mouse models. Omics analyses identified caveolae and their structural components (Cav1, -2 and cavin-1) as downregulated in imiquimod (IMQ)-treated mouse model of psoriasis. These observations were validated in patient samples of multiple types of psoriasis stratified by PASI score (plaque, inverse, guttate and nail) by IHC staining and quantified by QuPath image analysis software. Although all biopsy samples exhibited an inverse relationship with levels of Cav1, plaque psoriasis samples were the most pronounced. To assess whether reintroduction of Cav1 can alleviate some of the features associated with IMQ-induced model of psoriasis (increased skin thickness/scaling and upregulation of psoriasis associated markers), C57BL6 and K14cre-Cav1 knockout mice were treated with soluble caveolin scaffolding domain (CSD) peptide, in presence or absence of IMQ. We observed that Cav1ko mice exhibited a trend in increased skin thickness and expression of CD11b, CD14, IL-6, IL-12, IL-17a and TNFa, although to a lesser than IMQ-treated C57BL6 mice (Cav1 wild type). Moreover, topical CSD treatment decreased both skin thickness and scaling, as well as dampened upregulation of aforementioned inflammatory markers. Together, these data support the hypothesis that Cav1 is major pathophysiological target in psoriasis and introduce different approach to localized topical treatment of psoriasis by targeting structural components of the specialized membrane microdomains, such as caveolae.

Oxidative Stress Induced by High Salt Diet-Possible Implications for Development and Clinical Manifestation of Cutaneous Inflammation and Endothelial Dysfunction in Psoriasis vulgaris.

Although oxidative stress is recognized as an important effector mechanism of the immune system, uncontrolled formation of reactive oxygen and nitrogen species promotes excessive tissue damage and leads to disease development. In view of this, increased dietary salt intake has been found to damage redox systems in the vessel wall, resulting in endothelial dysfunction associated with NO uncoupling, inflammation, vascular wall remodeling and, eventually, atherosclerosis. Several studies have reported increased systemic oxidative stress accompanied by reduced antioxidant capacity following a high salt diet. In addition, vigorous ionic effects on the immune mechanisms, such as (trans)differentiation of T lymphocytes are emerging, which together with the evidence of NaCl accumulation in certain tissues warrants a re-examination of the data derived from in vitro research, in which the ionic influence was excluded. Psoriasis vulgaris (PV), as a primarily Th17-driven inflammatory skin disease with proven inflammation-induced accumulation of sodium chloride in the skin, merits our interest in the role of oxidative stress in the pathogenesis of PV, as well as in the possible beneficial effects that could be achieved through modulation of dietary salt intake and antioxidant supplementation.

The Levels of Wnt5a and Its Receptors Frizzled5 and Frizzled2 as Immunohistochemical Biomarkers of Severity of Psoriasis.

PurposePsoriasis is a systemic, chronic and inflammatory condition. The exact pathogenesis is unclear. The abnormal expression of Wnt5a pathway in psoriasis vulgaris has been confirmed. Whether it is related to the severity of psoriasis is unclear.MethodsThirty-eight skin lesions from psoriasis vulgaris patients and 22 healthy adult skin tissues were taken. The semi-quantitative immunohistochemistry score of Wnt5a, Frizzled5 and Frizzled2 was evaluated under a microscope by two independent dermatologists. Psoriasis area and severity index (PASI) score system was used to evaluate the disease severity.ResultsThe average PASI score of the patients was 16.25 ± 7.8, and the average duration of disease was 19.6 ± 10.4 months. Wnt5a, Frizzled5 and Frizzled2 were highly expressed in psoriasis lesions. The semi-quantitative immunohistochemistry scores of Wnt5a, Frizzled5 and Frizzled2 were positively correlated with PASI scores (r = 0.71, r = 0.46, r = 0.65, respectively, all P-value < 0.01), but not correlated with duration of disease (r = 0.11, r = 0.17, r = 0.29, respectively, all P-value > 0.05). There were significant positive correlations between Wnt5a and Frizzled5 (r = 0.57, P-value < 0.01), as well as Wnt5a and Frizzled2 (r = 0.59, P-value < 0.01).ConclusionWnt5a and its receptors play an important role in pathogenesis of psoriasis vulgaris and are positively correlated with the severity of psoriasis, and may be one of the immunohistochemical predictors of the severity of the disease.

RNA-seq reveal RNA binding protein GNL3 as a key mediator in the development of psoriasis vulgaris by regulating the IL23/IL17 axis

BackgroundPsoriasis is a systemic chronic inflammatory skin disorder that was prone to recurrence. The RNA binding protein GNL3 has an important function in maintaining the proliferative ability of stem cells, and its overexpression leads to apoptosis. GNL3 is expressed in the epidermis, however, its regulatory mechanism in psoriasis vulgaris is still poorly understood. ObjectiveTo identify the role of GNL3 in the pathogenesis of psoriasis vulgaris. Materials and methodsRNA-seq was performed to obtain the data of genes' expression and splicing events in Hela cells after shGNL3 and shCtrl was transferred. High quality results of differentially expressed genes (DEGs) and alternative splicing events (ASEs) were further attained by quality control and analysis. Through the functional enrichment analysis of DEGs and ASEs, the regulating effect of GNL3 was discussed, and the hypothesis was further confirmed in HaCat cells and psoriasis lesions. ResultsThe mRNA expression of IL23A in Hela cells was upregulated in GNL3 knockdown, and the ratio of ASE occurred in TNFAIP3 was increased. However, in HaCaT cells, the mRNA expression level of IL23A was downregulated in GNL3 knockdown, and the ratio of ASE of TNFAIP3 was decreased. Additionally, the results obtained in HaCaT cells was further validated in the lesional psoriatic skin. ConclusionGNL3 takes an important part in the development of psoriasis vulgaris by regulating the IL23/IL17 axis, which may serve as the basis of effective targeted treatment in future.

Serum Expression of IL-33 and ST2 in Patients with Psoriasis Vulgaris.

Psoriasis vulgaris (PsV) is an immune-mediated skin disease of unknown mechanism. Interleukin 33 (IL-33) is a member of IL-1 cytokine family and suppression of tumorigenicity 2 (ST2) is the specific ligand of IL-33. It has been found that IL-33 and ST2 are increased in psoriatic lesions, but the expression levels in serum and their relationship to clinical features are still unclear. The aim of this study is to assess IL-33, ST2, IL-17 and IL-5 serum levels as well as serum concentration of blood glucose and blood lipids in PsV patients and their relationship with clinical characteristics. Sixty-eight PsV samples and 60 healthy individuals were recruited. Serum levels of IL-33, ST2, IL-17 and IL-5 were measured by enzyme-linked immunosorbent assay and blood glucose and blood lipid were assayed by automatic biochemical analyzer. Serum levels of IL-33, ST2, IL-17 and IL-5 were increased significantly in PsV patients compared with controls (P<0.01). Cytokines were overexpressed in PsV patients during active stages compared with controls (P<0.05). Expression levels of IL-33, ST2 and IL-17 confirmed a significance in different severity groups of PsV patients (P<0.05). Serum concentration of triglyceride (TG) was also increased compared with controls (P=0.024). IL-33 levels were positively correlated with total cholesterol (TC) levels (r=0.319, P=0.008). IL-33/ST2 could generally reflect the activity and disease severity in PsV patients, which indicates that the IL-33/ST2 signaling pathway plays an important role in the pathogenesis of PsV.

Enhanced serum interferon-lambda 1/interleukin-29 levels in patients with psoriasis vulgaris

BackgroundInterferon (IFN)-λ1, also named Interleukin (IL)-29, is a new member of the Type III IFN or IFN-λ family. IL-29 plays an important role in the pathogenesis of many types of autoimmune and inflammatory diseases. ObjectiveTo study the role of IL-29 in the pathogenesis of psoriasis vulgaris. MethodsThe authors detected the serum levels of IL-29 in forty-one patients with psoriasis vulgaris, twenty-three patients with atopic dermatitis and thirty-eight age and gender-matched controls by sandwich Enzyme-Linked Immunosorbent Assay (ELISA). The effects of IL-29 on the expression of cytokines, such as IL-6, IL-17, IL-8, IL-4, IL10, Interferon (IFN-γ) and Tumor Necrosis Factor-α (TNF-α), in PBMCs and HaCat cells were determined by real-time quantitative PCR. ResultsOur data indicated that serum IL-29 levels were significantly elevated in patients with psoriasis vulgaris when compared with atopic dermatitis patients and the control group. Moreover, Serum levels of IL-29 were closely associated with the severity of psoriasis vulgaris. Furthermore, IL-29 up-regulated the mRNA expression levels of IL-6, IL-17 and TNF-α in PBMCs from psoriasis vulgaris patients. In addition, IL-29 enhanced the IL-6 and IL-8 expression from the HaCat cells. ConclusionThis study provides the first observations on the association of IL-29 and psoriasis vulgaris and showed elevated IL-29 serum levels. The authors suggest that IL-29 may play a role in the pathogenesis of psoriasis vulgaris.

Involvement of the cytokine TWEAK in the pathogenesis of psoriasis vulgaris, pustular psoriasis, and erythrodermic psoriasis

Psoriasis is a common chronic inflammatory dermatitis in which various cytokines play a detrimental role. The cytokine tumor necrosis factor-related weak inducer of apoptosis (TWEAK) is involved in the pathogenesis of multiple inflammatory disorders. However, the potential role of TWEAK in various subtypes of psoriasis has not been studied in depth. To investigate whether the levels of TWEAK are associated with clinical traits and the levels of some known psoriasis-related cytokines, such as interleukin (IL)-17A, IL-22, interferon (IFN)-γ, and IL-36γ, 20 patients with psoriasis vulgaris (PV), 8 patients with pustular psoriasis (PP), 8 patients with erythrodermic psoriasis (EP), and 20 healthy controls (HCs) were recruited into this study. The levels of serum cytokines were detected by commercial enzyme-linked immunosorbent assay kits. The average levels of TWEAK, IL-17A, IL-22, IFN-γ, and IL-36γ were significantly higher in the psoriasis groups than in the HC group. Furthermore, there was a statistically significant correlation between TWEAK and IL-17A/IFN-γ in PV and IL-36γ in EP, but there was no correlation between TWEAK and IL-22 in any subtype of psoriasis. This study suggests that TWEAK may have a role in the pathogenesis of PV, PP, and EP via synergy with IL-17A, IFN-γ, or IL-36γ, but not with IL-22.

Correlation of plasma vitamin d receptors with the severity of psoriasis vulgaris

Introduction: Psoriasis vulgaris is still a major problem in the field of dermatology. Until recently, the exact cause of psoriasis is still being debated. In recent years research has been carried out on vitamin D and its role in the immune system, especially in psoriasis. Vitamin D cannot be separated from the role of VDR. The study aims to evaluate correlation between VDR plasma levels and the severity of psoriasis vulgaris.Method: Study design using a cross-sectional design to determine the correlation of vitamin D levels in plasma with the severity of psoriasis vulgaris calculated using the Psoriasis Area and Severity Index (PASI) score.Result: This study included 47 study participants who had psoriasis vulgaris, consisting of 30 (63.8%) men and 17 (36.2%) women with a mean age of 44.66 years. The mean PASI score was 6.904, while the mean plasma VDR level was 30.328 ng/ml. Spearman correlation shows a strong negative correlation (r = - 0.979; p &lt;0.001) between plasma VDR levels and PASI scores in psoriasis vulgaris patients.Conclusion: Vitamin D plays a role in regulating the growth and differentiation of keratinocytes and influences dendritic cells and T lymphocytes' immune function so that low vitamin D levels have essential implications in the pathogenesis of psoriasis vulgaris. In performing its function, vitamin D must bind to VDR and form a complex. In this study, it was found that there was a strong negative correlation between plasma VDR levels and PASI scores, so it can be concluded that low plasma VDR levels correlate with high degrees of psoriasis vulgaris severity and vice versa.

Correlation analysis between IL-35, IL-36γ, CCL27 and psoriasis vulgaris

Objective Evaluating the serum level of IL-35, IL-36γ and CCL27 cytokines expression in patients with psoriasis and to explore their correlation with disease severity. To explore the role of these cytokines in the pathogenesis of psoriasis vulgaris and to guide clinical practice. Methods Thirty patients with psoriasis vulgaris (PV) were treated with routine drug treatment for7 weeks, and 30 healthy controls were used as control group. Peripheral blood of the PV group before and after treatment and control group were detected by double-antibody sandwich ELISA. The expression levels of IL-35, IL-36γ and CCL27 in peripheral blood were analyzed statistically. Results The expression of IL-35 in the peripheral blood of the pre-PV group (187.54 ± 172.41) was significantly lower than that of the control group (310.52 ± 174.22) and the PV treatment group (417.75 ± 47.07). The level of IL-36γ in peripheral blood of pre-PV group (295.11 ± 27.91) was higher than that of control group (155.40 ± 45.66) and PV treatment group (209.86 ± 27.91). The level of CCL27 in peripheral blood of patients pre-PV treatment (479.06 ± 285.80) was significantly higher than that of the control group (341.53 ± 98.72) and the group after PV treatment (316.56 ± 245.53). There was a negative correlation between IL-35 and IL-36γ levels in serum (r= –0.826, p < .001); IL-36γ was positively correlated with CCL27 level (r = 0.906, p < .001); IL-35 and CCL27 levels were negative correlation (r= –0.810, p < .001). Conclusion IL-36γ and CCL27 may be involved in the pathogenesis of psoriasis as a pro-inflammatory factor. IL-35 may be involved in the pathogenesis of psoriasis as an anti-inflammatory factor.

Skin tissue expression and serum level of thymic stromal lymphopoietin in patients with psoriasis vulgaris

Thymic stromal lymphopoietin (TSLP) is known to be associated with allergic diseases. It is also suggested that TSLP has a role in autoimmune diseases such as psoriasis; however, the associated pathways remain unknown. There is currently little information on TSLP in psoriasis vulgaris. We investigated TSLP expressions on lesional and non-lesional skin of psoriasis vulgaris patients using reverse transcription- polymerase chain reaction. TSLP level was also investigated in serum from psoriasis vulgaris patients compared to healthy control using enzyme-linked immunosorbent assay. TSLP expression was higher in lesional skin (1.90) compared to non-lesional skin (1.76); however, the difference was not statistically significant (P>0.05). TSLP serum levels were significantly higher in psoriasis patients (287.40 pg/dL) as compared to controls (114.70 pg/dL) (P<0.05). This study concluded that TSLP levels in the serum of psoriasis vulgaris patients are higher than controls. TSLP was also found in keratinocyte of psoriasis patients, the expression was higher in the lesional compared to non-lesional skin; however, this difference is statistically insignificant. These findings suggest that TSLP may play a role in the pathogenesis of psoriasis vulgaris, but its exact role remains unclear.

The polymorphism rs4696480 in the TLR2 gene is associated with psoriasis patients in the Turkish population

BackgroundToll-like receptors (TLRs) have an important role in the host defense. Recent studies demonstrated that TLR polymorphisms might have a role in the pathogenesis of psoriasis vulgaris. The aim of this study was to indicate whether TLR2 rs11938228 and rs4696480 were associated with susceptibility to psoriasis in the Turkish population. MethodsThis case-control study included 140 psoriasis patients and 250 controls. Genotyping of 2 rs11938228 and rs4696480 SNPs of TLR2 were determined using LightSNiP Kit (Roche Diagnostic, GmBH, Mannheim, Germany). ResultsOur results demonstrated that the TLR2-rs4696480 AA genotype seemed to have a higher risk for psoriasis [crude 95% CI: 1.495–4.514, and p < 0.001, adjusted 95% CI: 1.349–4.292, and p = 0.003] while as TLR2-rs11938228 polymorphism has not shown any significant association with the risk of psoriasis [p > 0.005]. There was no statistically significant difference between the mean age, gender, onset age, and PASI level and genotypes for rs11938228 and rs4696480 polymorphisms (p > 0.05). ConclusionsThe SNP rs4696480 of TLR2 may have significant effects on the heritability of psoriasis in the Turkish population.

Serum Level of Periostin and Cardiac Function in Patients with Psorasis

Psoriasis is a common chronic immune mediated relapsing and remitting, inflammatory skin diseases causing significant impairment of quality of life, at least to the same extent as other major medical diseases. About 2% of the population in Europe and the United States are affected by psoriasis. the present work aim to asses serum level of periostin in psoriatic patients, in an attempt to elucidate its role in the disease pathogenesis in psoriatic patient. fifty adult patients with psoriasis vulgaris (PV) as a disease control and30 healthy controls were determined their serum level of periostin using An enzyme-linked immunosorbent assay. serum levels of periostin were significantly increased in psoriatic patients, with a significant positive correlation to the disease severity when compared to the healthy controls. In conclusion, periostin may play a role in the pathogenesis of PV.

Advances in Understanding the Immunological Pathways in Psoriasis.

Psoriasis vulgaris is a chronic, immune-mediated, inflammatory, polygenic skin disorder affecting approximately 2% of the population. It has a great impact on quality of life; patients often experience depression, anxiety, stigma as well as suicidal behavior. Even though psoriasis is one of the most studied dermatological conditions, the pathogenesis of the disease is still not completely elucidated. The complex interactions between keratinocytes, dendritic cells, T-lymphocytes, neutrophils and mast cells are responsible for the histopathological changes seen in psoriasis. The pathogenic model leading to the formation of psoriatic plaques has however evolved a lot over the years. There is now enough evidence to support the role of interleukin (IL) -23, IL-17, IL-22, T helper (Th) -17 cells, Th-22 cells, T regulatory cells, transforming growth factor (TGF)-β1 and IL-10 in the pathogenesis of the disease. Moreover, several inflammatory and anti-inflammatory molecules are currently being investigated, some of them showing promising results. The aim of this paper is to look over the most recent advances in the immunological pathways involved in the pathogenesis of psoriasis vulgaris.

Increased dermal expression of chromatin-associated protein HMGB1 and concomitant T-cell expression of the DNA RAGE in patients with psoriasis vulgaris.

PurposePsoriasis vulgaris (PV) is an autoimmune-related chronic inflammatory disease of the skin, with both vascular and metabolic effects. Aggravating factors have been identified that initiate and maintain inflammation, including expression of Th1-, Th17-, and Th22-cell derived cytokines. Recently, we showed that the evolutionarily ancient and highly conserved damage-associated molecular pattern molecule “high mobility group box 1 (HMGB1)” is significantly increased in the serum of PV patients with disease progression and is decreased under standard therapies.Materials and methodsTo better understand the role of HMGB1 in the pathogenesis of PV, we recruited 22 untreated psoriatic patients with either mild or severe disease, defined by the Psoriasis Area Severity Index. We assessed HMGB1 and receptor for advanced glycation end products (RAGE) expression in the skin by immunohistochemistry and analyzed the immune-phenotype of Treg and Th17 cells by flow cytometry.ResultsWe found increased staining for HMGB1 in the dermis of psoriatic plaques in comparison to uninvolved skin of patients with PV. In addition, the major histocompatibility complex class III-encoded DNA and HMGB1 RAGE, induced by HMGB1, were highly expressed on psoriatic CD8+ T cells and CD4+ Treg. High expression of HMGB1 in the lesional skin was associated with even higher expression of its receptor, RAGE, on the cell surface of keratino-cytes in patients with severe PV.ConclusionThe presence of HMGB1 and RAGE signaling may impact orchestration of chronic inflammation in PV which might have implications for Treg and Th17 cells.