The influence of ustekinumab on expression of
 STAT1
 ,
 STAT3
 ,
 STAT4
 ,
 SOCS2
 , and
 IL17
 in patients with psoriasis and in a control

Grabarek, Beniamin Oskar; Krzaczyński, Jakub; Strzałka‐Mrozik, Barbara; Wcisło‐Dziadecka, Dominika; Gola, Joanna

doi:10.1111/dth.13029

Cited by 8 publications

(4 citation statements)

References 31 publications

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“…Moreover, these mice also failed to develop psoriasis-like inflammation suggesting the essential role of STAT3 in the production of inflammatory cytokines and development of psoriatic lesions [85]. The key role of STAT3 in the development of psoriatic lesion is further supported by a study showing that treatment with ustekinumab (a monoclonal antibody that targets IL-12 and IL-23 and is used clinically for psoriasis) down-regulates the expression of STAT3 in psoriatic patients [86].…”

Section: Il-17 Nf-kb and Signal Transducer And Activator Of Transcrmentioning

confidence: 95%

Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms

Liu

2019

Bioscience Reports

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Koebner phenomenon refers to the emergence of new psoriatic lesions in the healthy skin regions following an injury/trauma to psoriatic patients. The occurrence of psoriatic lesions at unusual areas of the body regions such as on penis, around eyes and on keloids suggest that the Koebner phenomenon may be responsible for these lesions. A number of agents/triggers have been reported to induce the development of new psoriatic lesions in healthy skin areas and these include, tattooing skin, radiations, skin incision, viral infections and striae etc. The different mechanisms that contribute in inducing the development of new psoriatic lesions as Koebernization include the involvement of mast cell-derived inflammatory mediators such as tryptase, IL-6, IL-8, IL-17, and IL-36γ. Moreover, an increased expression of nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) also contribute in Koebernization. Apart from these, there is a critical role of α 2 β1 integrins, S100A7 (psoriasin) and S100A15 (koebnerisin), change in the ratio of CD4+/CD8+ T cells, down-regulation of mechanosensitive polycystin 1 protein, decrease in inflammation controlling atypical chemokine receptor 2 (ACKR2), reduced expression of N-methyl-d-aspartate (NMDA) receptors (NMDARs) on the keratinocytes and increase in levels of chemokines (CXCL8 and CCL20) in inducing formation of new psoriatic lesions. The present review discusses the role of Koebner phenomenon in the development of new psoriatic lesions. Moreover, it also describes the mechanisms involved in Koebernization in the form of discussion of different key targets that may be potentially modulated pharmacologically to attenuate/halt the development of new psoriatic lesions.

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Section: Il-17 Nf-kb and Signal Transducer And Activator Of Transcrmentioning

confidence: 95%

Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms

Liu

2019

Bioscience Reports

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“…STAT1 and STAT3 are critical transcription regulatory factors that control cell growth, programmed cell death pathways, and in ammatory responses. The expression levels of STAT1 and STAT3 are higher in patients with psoriasis vulgaris compared to healthy individuals 33 . The balanced regulation between STAT3 and STAT1 controls the expression of IL-22 and IL-17A, in uencing skin in ammation 34 .…”

Section: Discussionmentioning

confidence: 91%

Bioinformatics analysis of the shared pathogenesis of psoriasis and Crohn's disease

Yang

Liu

et al. 2023

Preprint

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Background There exists a bidirectional causal relationship between psoriasis and Crohn's disease, where psoriasis can increase the risk of Crohn's disease, and Crohn's disease can also increase the risk of psoriasis. However, the underlying mechanism of their co-occurrence remains unclear. This study aims to explore the pathogenesis of psoriasis combined with Crohn's disease through bioinformatics analysis. Methods Psoriasis skin tissue data (GSE117239) and Crohn's disease intestinal tissue data (GSE95095) were downloaded from the GEO database. The imma R package and Weighted Gene Co-expression Network Analysis (WGCNA) were used to identify common differentially expressed genes. Further analyses included Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, construction of a protein-protein interaction (PPI) network, screening and validation of hub genes, prediction and validation of hub transcription factors (TFs), and additional analysis of the diagnostic value of hub genes, as well as prediction of therapeutic drugs. Results 99 common differentially expressed genes were identified for psoriasis and Crohn's disease. The results of GO and KEGG enrichment analysis were focused on inflammation and energy metabolism processes. 6 hub genes were screened, namely MMP9, CXCR2, CXCL1, CXCL10, HMGCS2, and PPARGC1A. Some of these hub genes showed high diagnostic value. Three hub TFs were predicted and validated, which were STAT1, STAT3, and IRF1. Based on these hub genes and hub TFs, a total of 66 drugs were predicted, with some drugs overlapping with the existing therapeutic drugs for psoriasis or Crohn's disease. Conclusions This study revealed the potential common pathogenesis of psoriasis and Crohn's disease through bioinformatics analysis. These hub genes, hub TFs, and predicted drugs may provide new perspectives for further mechanistic research.

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“…For instance, STAT1, a transcription hub, inhibits the expression of metalloproteinases-3, influencing the cell adhesion molecule pathway and blood vessel formation [ 44 ]. STAT1 also affects the activity of the IL-22 promoter, which plays an important role in tissue repair and inflammatory responses [ 45 , 46 ]. ZFX acts as an important regulator in the proliferation and migration of keratinocytes in skin wound healing.…”

Section: Resultsmentioning

confidence: 99%

Generating detailed intercellular communication patterns in psoriasis at the single-cell level using social networking, pattern recognition, and manifold learning methods to optimize treatment strategies

Xiong,

Li,

Bai

et al. 2024

Aging

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Psoriasis, a complex and recurrent chronic inflammatory skin disease involving various inflammatory cell types, requires effective cell communication to maintain the homeostatic balance of inflammation. However, patterns of communication at the single-cell level have not been systematically investigated. In this study, we employed social network analysis tools, pattern recognition, and manifold learning to compare molecular communication features between psoriasis cells and normal skin cells. Utilizing a process that facilitates the discovery of cell type-specific regulons, we analyzed internal regulatory networks among different cells in psoriasis. Advanced techniques for the quantitative detection of non-targeted proteins in pathological tissue sections were employed to demonstrate protein expression. Our findings revealed a synergistic interplay among the communication signals of immune cells in psoriasis. B-cells were activated, while Langerhans cells shifted into the primary signaling output mode to fulfill antigen presentation, mediating T-cell immunity. In contrast to normal skin cells, psoriasis cells shut down numerous signaling pathways, influencing the balance of skin cell renewal and differentiation. Additionally, we identified a significant number of active cell type-specific regulons of resident immune cells around the hair follicle. This study unveiled the molecular communication features of the hair follicle cell-psoriasis axis, showcasing its potential for therapeutic targeting at the single-cell level. By elucidating the pattern of immune cell communication in psoriasis and identifying new molecular features of the hair follicle cell-psoriasis axis, our findings present innovative strategies for drug targeting to enhance psoriasis treatment.

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The influence of ustekinumab on expression of STAT1 , STAT3 , STAT4 , SOCS2 , and IL17 in patients with psoriasis and in a control

Cited by 8 publications

References 31 publications

Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms

Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms

Bioinformatics analysis of the shared pathogenesis of psoriasis and Crohn's disease

Generating detailed intercellular communication patterns in psoriasis at the single-cell level using social networking, pattern recognition, and manifold learning methods to optimize treatment strategies

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