Psoriasis Pathogenesis and Treatment

Rendón, Adriana; Schäkel, Knut

doi:10.3390/ijms20061475

Cited by 1,391 publications

(1,343 citation statements)

References 217 publications

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“…Psoriasis is a chronic inflammatory skin disease characterized by the hyperproliferation of keratinocytes and infiltration of inflammatory cells. It affects about 2% of the population worldwide, but the rate varies according to region [1]. The molecular mechanisms of psoriasis are complicated and unclear, but many studies have indicated that psoriasis is an immune-mediated disease.…”

Section: Introductionmentioning

confidence: 99%

Immune Regulation of TNFAIP3 in Psoriasis through Its Association with Th1 and Th17 Cell Differentiation and p38 Activation

Jiang

Wang

Zheng

et al. 2020

Journal of Immunology Research

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Background. Psoriasis is an immune-mediated chronic inflammatory skin disorder in which the dysregulation of immune cells plays an important role in its development. Tumor necrosis factor- (TNF-) α antagonists affect the immune repertoire, while TNF-α-induced protein 3 (TNFAIP3) has a protective role against the deleterious effects of inflammation and participates in immune regulation. Objective. We investigated the immune regulation of TNFAIP3 in the pathogenesis of psoriasis and determined whether it is involved in the antipsoriatic effect of TNF-α antagonists. Methods. mRNA levels were evaluated in blood from patients with moderate-to-severe psoriasis. The effects of TNF-α antagonists were examined in a mouse imiquimod- (IMQ-) induced psoriasis-like dermatitis model. In the mouse model, TNFAIP3 mRNA expression was determined using RT-PCR. Serum levels of IL-17A, IL-23, IFN-γ, TNF-α, phosphorylated ERK1/2, p38, and JNK were measured using ELISA. The proportion of Th1 and Th17 cells in mouse spleens was analyzed using flow cytometry. Results. mRNA expression levels of TNFAIP3 in the blood were significantly lower in patients with moderate and severe psoriasis (mean±SD=0.44±0.25) compared with normal subjects (mean±SD=1.00±0.82) (P<0.01). In the mouse model, IMQ downregulated TNFAIP3 expression levels, which were increased after TNF-α antagonist treatment (P<0.05). Serum levels of Th17 cytokines (IL-17A and IL-23) and Th1 cytokines (IFN-γ and TNF-α) were significantly higher in the IMQ and IMQ/rat IgG1 groups compared with the control group, and the application of TNF-α antagonists significantly decreased the levels of inflammatory cytokines (P<0.01). Notably, phosphorylated p38 levels were increased in the IMQ and IMQ/rat IgG1 groups compared with the control group but were downregulated by treatment with TNF-α antagonists (P<0.05). Th1 and Th17 cells were significantly increased in the IMQ group compared with the control group (P<0.01). Conclusion. TNFAIP3 downregulation associated with Th1 and Th17 cell differentiation and p38 activation might contribute in part to the mechanism of immune dysfunction in psoriasis. TNF-α antagonists might partly exert their effects on psoriasis via this pathway.

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Section: Introductionmentioning

confidence: 99%

Immune Regulation of TNFAIP3 in Psoriasis through Its Association with Th1 and Th17 Cell Differentiation and p38 Activation

Jiang

Wang

Zheng

et al. 2020

Journal of Immunology Research

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“…Psoriasis is a chronic inflammatory skin condition that is also likely manifested in patients with a genetic predisposition who are acted on by exogenous factors. While there are various subtypes of psoriasis, all are characterized by erythematic, and often pruritic, plaques . Psoriasis is predominantly thought to be caused by an inappropriate activation of the cutaneous immune system against a perceived pathogen .…”

Section: Addressing the Skin Microflora To Combat Disease Statesmentioning

confidence: 99%

The role of topical probiotics in skin conditions: A systematic review of animal and human studies and implications for future therapies

Knackstedt

Gatherwright

2019

Experimental Dermatology

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There is increasing evidence that the intestinal microbiome plays an important role in modulating systemic inflammation and disease. Oral probiotics can modulate the intestinal microbiome and have demonstrated to be efficacious in treating topical skin conditions, such as atopic dermatitis, acne and rosacea. By proxy, exogenous application to the skin of probiotics should also promote a positive bacterial balance to mitigate or potentially eliminate pathologic conditions. The goal of this article was to provide a systematic review of studies that have investigated the role of topical probiotics in mitigating skin conditions. Additionally, skin conditions where dysbiosis has been identified but topical probiotics have not been investigated are discussed. We hope this review both analyses the evidence for the role that topical probiotics could play in topical skin conditions and highlights additional areas in need of research and exploration.

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“…Psoriasis is treated by conventional drugs such as methotrexate, cyclosporine, retinoids and dimethyl fumarate and apremilast or by biologics such as anti TNF-α and IL23/IL17 blockers [1,2,3] ; however, in such treatments there are limitation suggesting the wisdom to develop new interventions [4,5,6] .…”

Section: Introductionmentioning

confidence: 99%

Optimization of psoriasis – like mouse models: A comparative study

Karamani

Antoniadou

Dimou

et al. 2020

Preprint

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Psoriasis, a common chronic, autoimmune, inflammatory, relapsing disease should benefit from reliable and human relevant animal models in order to pre-clinically test drugs and approach their mechanism of action. Due to ease of use, convenience and low cost, imiquimod (IMQ)induced psoriasis-like model is widely utilized; however, are all mouse strains equivalent, is the hairless mouse utilizable and can the imiquimod model be further optimized? Under similar experimental conditions, common mouse strains (BALB/c, C57BL/6J, ApoE) and a new hairless strain (ApoE/SKH-hr2) as well as several inducers (IMQ, IMQ + Acetic Acid (AcOH) topical and IMQ +AcOH systemic) were compared by clinical, histopathological, biophysical and locomotor activity assessment. Results showed that BALB/c mice yielded optimal psoriasislike phenotype with IMQ+AcOH topical treatment, C57BL/6J moderate, ApoE mild, while the ApoE/SKH-hr2 mice due to Munro abscess absence in histopathology analysis left doubts about the psoriasis-like acquisition. The locomotor activity of BALB/c mice treated with IMQ, IMQ+AcOH topically and IMQ+AcOH systemically, showed with all treatments, a decreased covered distance and rearing and an increased immobility. In conclusion, BALB/c appears an optimal psoriasis-like model when utilizing IMQ+AcOH topical application.Abbreviations: psoriasis area and severity index (PASI), imiquimod (IMQ), acetic acid AcOH, transepidermal water loss (TEWL), psoriatic histopathology score (PHS), T helper cells (CD4)

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Psoriasis Pathogenesis and Treatment

Cited by 1,391 publications

References 217 publications

Immune Regulation of TNFAIP3 in Psoriasis through Its Association with Th1 and Th17 Cell Differentiation and p38 Activation

Immune Regulation of TNFAIP3 in Psoriasis through Its Association with Th1 and Th17 Cell Differentiation and p38 Activation

The role of topical probiotics in skin conditions: A systematic review of animal and human studies and implications for future therapies

Optimization of psoriasis – like mouse models: A comparative study

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