Anti-TNF-α monoclonal antibody reverses psoriasis through dual inhibition of inflammation and angiogenesis

Liu, Yu; Yang, Guoyou; Zhang, Junfeng; Xing, Kaiyan; Dai, Lei; Cheng, Lin; Deng, Jie; Shi, Gang; Li, Chunlei; Su, Xiaolan; Zhang, Shuang; Yang, Yang; Li, Jia; Yu, Dechao; Xiang, Rong; Wei, Yuquan; Deng, Hongxin

doi:10.1016/j.intimp.2015.07.036

Cited by 34 publications

(26 citation statements)

References 44 publications

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“…TNF‐α inhibitors are highly effective for the treatment of psoriasis . We have confirmed that TNF‐α monoclonal antibody IBI303 could achieve good effects in the treatment of psoriasis by anti‐inflammation and inhibiting angiogenesis . However, the degree of immunosuppression induced by blocking TNF‐α can lead to adverse events .…”

Section: Resultsmentioning

confidence: 72%

IL‐35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells

Wang

Mao

Zhang

et al. 2017

J Cellular Molecular Medi

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Interleukin-35 (IL-35), a member of the IL-12 family, functions as a new anti-inflammatory factor involved in arthritis, psoriasis, inflammatory bowel disease (IBD) and other immune diseases. Although IL-35 can significantly prevent the development of inflammation in many diseases, there have been no early studies accounting for the role of IL-35 recombinant protein in IBD and psoriasis. In this study, we assessed the therapeutic potential of IL-35 recombinant protein in three well-known mouse models: the dextransulfate sodium ( Further analysis demonstrated that IL-35 recombinant protein may regulate inflammation through promoting the secretion of IL-10 and inhibiting the expression of pro-inflammatory cytokines such as IL-6, TNF-a and IL-17 in acute colitis model. In addition, lower dose of IL-35 recombinant protein could achieve long-term treatment effects as TNF-a monoclonal antibody did in the psoriasis mouse. In summary, the remarkable therapeutic effects of IL-35 recombinant protein in acute colitis and psoriasis mouse models indicated that IL-35 recombinant protein had a variety of anti-inflammatory effects and was expected to become an effective candidate drug for the treatment of inflammatory diseases.

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Section: Resultsmentioning

confidence: 72%

IL‐35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells

Wang

Mao

Zhang

et al. 2017

J Cellular Molecular Medi

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“…TNF superfamily cytokines are increasingly recognized as key modulators of angiogenesis. TNF-α is not only involved with angiogenesis 48 49 50 51 , but also enhances the motility and invasiveness of prostatic cancer cells 52 . It is possible that down-regulation of TNF-α, mediated by let-7b, contributes to the suppression of angiogenesis and PC-3 mobility.…”

Section: Discussionmentioning

confidence: 99%

miRNA let-7b modulates macrophage polarization and enhances tumor-associated macrophages to promote angiogenesis and mobility in prostate cancer

Wang

et al. 2016

Sci Rep

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Macrophage polarization is a highly plastic physiological process that responds to a variety of environmental factors by changing macrophage phenotype and function. Tumor-associated macrophages (TAMs) are generally recognized as promoting tumor progression. As universal regulators, microRNAs (miRNAs) are functionally involved in numerous critical cellular processes including macrophage polarization. Let-7b, a miRNA, has differential expression patterns in inflamed tissues compared with healthy controls. However, whether and how miRNA let-7b regulates macrophage phenotype and function is unclear. In this report, we find that up-regulation of let-7b is characteristic of prostatic TAMs, and down-regulation of let-7b in TAMs leads to changes in expression profiles of inflammatory cytokines, such as IL-12, IL-23, IL-10 and TNF-α. As a result, TAMs treated with let-7b inhibitors reduce angiogenesis and prostate carcinoma (PCa) cell mobility. Let-7b may play a vital role in regulating macrophage polarization, thus modulating the prognosis of prostate cancer.

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“…An increase in the skin wound healing process and Koebner reaction in the psoriatic patients suggest that the proliferation of keratinocytes is not inhibited appropriately. Accordingly, scientists have explored the expression pattern of NMDARs on the keratinocytes in the presence of TNF-α, a cytokine with a prominent role in psoriasis [115]. Using gene expression analysis, the greatest reduction in the expression of NMDA-R2C was found in TNF-α-exposed keratinocytes and the apparently increased proliferation of keratinocytes was attributed to the decrease in the expression of NMDA-R2C.…”

Section: Down-regulation Of Nmdarmentioning

confidence: 99%

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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Anti-TNF-α monoclonal antibody reverses psoriasis through dual inhibition of inflammation and angiogenesis

Cited by 34 publications

References 44 publications

IL‐35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells

IL‐35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells

miRNA let-7b modulates macrophage polarization and enhances tumor-associated macrophages to promote angiogenesis and mobility in prostate cancer

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

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