Predominant role of innate pro-inflammatory cytokines in vitiligo disease

Gholijani, Nasser; Yazdani, Maryam; Dastgheib, Ladan

doi:10.1007/s00403-019-01996-9

Cited by 49 publications

(44 citation statements)

References 41 publications

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“…These results demonstrate that, although TLR3 agonism induces several signaling cascades, including activation of IKK/nuclear factor kB (NF-kB) signaling, IKK/TBK1 signaling, and mitogen-activated protein kinase (MAPK) signaling (Kawasaki and Kawai, 2014), JAK1-dependent signaling is the major driver of the hyperinflammatory and wasting phenotypes in this setting. Our findings may be of critical significance to individuals with T21 because they point to dysregulated antiviral responses and identify therapeutic strategies for comorbidities more prevalent in this population, where IFN signaling could drive pathology, such as autoimmune skin conditions (Gholijani et al, 2020), arthropathy (Foley et al, 2019;Nehmar et al, 2018), and even AD (Mastrangelo et al, 2009;Roy et al, 2020;Taylor et al, 2014). The therapeutic potential of JAK inhibition in DS is already under investigation in a clinical trial (NCT04246372), and we showed recently that the JAK1/ JAK3 inhibitor tofacitinib has therapeutic benefits for alopecia areata in DS (Rachubinski et al, 2019).…”

Section: Discussionmentioning

confidence: 87%

JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model of Down Syndrome

et al. 2020

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Section: Discussionmentioning

confidence: 87%

JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model of Down Syndrome

et al. 2020

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“… 40 Various inflammatory cytokines (IL-1, IL-6, TNF-α, IL-6, and IL-17) have a key role in skin depigmentation, while the level of TGF-β indicated reversible state. 6 , 41 …”

Section: Discussionmentioning

confidence: 99%

Decreased levels of interleukin 27 in the serum of vitiligo patients

Hosseini

Gholijani

Chenari

et al. 2020

Anais Brasileiros de Dermatologia

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Background Vitiligo is a common skin disorder in which melanocytes are destroyed by auto-reactive immune responses. The loss of melanocytes results in the appearance of depigmented areas in different parts of the body. Cytokines have remarkable roles in the pathogenesis of vitiligo, such as IL-1, IL-6, and TNF-α; interleukin 27 (IL-27) is a new member of the IL-6/IL-12 family, mainly released by activated antigen-presenting cells. IL-27 has been suggested to function as a pro-inflammatory as well as an anti-inflammatory cytokine. Altered concentrations of IL-27 have been shown in various auto-immune diseases such as multiple sclerosis, rheumatoid arthritis, and psoriasis. No studies have been conducted to determine the expression of this cytokine in vitiligo patients. Objective The objective of this study was to determine the serum concentration of IL-27 in vitiligo patients and compare it with normal individuals. Methods The serum concentration of IL-27 in 79 vitiligo patients was evaluated in comparison to 45 healthy controls using ELISA assay. Results Results showed decreased concentration of IL-27 in vitiligo patients as compared with healthy subjects ( p = 0.026). Furthermore, no correlation between IL-27 concentrations and disease parameters such as vitiligo severity and the extension of the depigmented area was observed. Study limitation A larger sample size would be more recommended for this study. Conclusion The reduction in the serum levels of IL-27 in vitiligo patients compared to normal subjects suggested the possible anti-inflammatory role of this cytokine in vitiligo. Thus, IL-27 may be considered as a new target for the manipulation of the immune system in vitiligo patients.

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“…Além disso, dados experimentais indicam que a IL-12 atua na diferenciação de células Th1, enquanto que IL-1β, IL-6 e IL-23 estão particularmente envolvidas no desenvolvimento, proliferação e sobrevivência de células Th17. 26 A bradicinina é outra citocina inflamatória (ou pró-inflamatória), com estrutura nonapeptídica e que conta com 2 receptores: B1 e B2. Os receptores B1 são estimulados por qualquer lesão tecidual, enquanto que os receptores B2, localizados na superfície das células endoteliais, liberam prostaglandinas e NO, quando ativados.…”

Section: Citocinasunclassified

Pathophysiological Aspects of Inflammation and Drug Design: an Updated Overview

Etienne¹,

Viegas²,

Viegas³

2021

Rev. Virtual Quim.

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Inflammation is a natural response of the organism to damage, injury or tissue lesions caused by foreign matter, trauma, infection, immune reactions and tissue necrosis. As being a protection response, inflammation onset and progression involve immune cells, blood vessels and a number of molecular mediators. Once the inflammatory process begins, it is associated to the release of chemical substances, such as cytokines and chemokines (e.g. TNF-α, lipoxynes, kinins, prostaglandins, leukotrienes) and cellular signaling proteins in the tissue environment and migration cells. As a result of a wealth knowledge through decades of research in fields like physiology, pharmacology and molecular biology, since 1980's a more comprehensive vision emerges, recognizing the inflammatory process as a complex result of an interconnected biochemical and cellular events, acting as a driving force associated to many chronic diseases, including obesity, diabetes, arteriosclerosis, cancer and neurodegenerative disorders such as Parkinson's (PD) and Alzheimer's diseases (AD), responsible by severe social-economic impacts in population worldwide. During the last decades, the therapeutics and research of new drugs have been focused on the search and development of lower toxic non-steroidal anti-inflammatory agents, that could act mainly towards the arachidonic acid cascade, more specifically in the inhibition of COX-1, COX-2 and 5-LOX enzymes and modulating the production of prostaglandins, thromboxane and leukotrienes. More recently, the urge of more efficient, low toxic and more specific drugs to certain inflammatory conditions has directing the research for the development of novel drugs capable to act towards other inflammatory mediators, such as interleukins, TNF-α, nitric oxide, kinase proteins, PPARs, endocannabinoid system, opioid receptors and proteins related to apoptosis, leading to the discovery of new drug candidates with different mechanisms of action, could also act in multiple inflammatory targets. A inflamação é uma reação natural do organismo a danos, injúria ou lesões teciduais devidas à presença de um corpo estranho, trauma, infecções, reações imunológicas e necrose tecidual. Por ser uma resposta protetora, a instalação e progressão da inflamação envolve células imunes, vasos sanguíneos e uma série de mediadores moleculares. Uma vez iniciado, o processo inflamatório está associado à liberação de substâncias químicas como as citocinas e quimiocinas (e.g. TNF-α, lipoxinas, cininas, prostaglandinas, leucotrienos) e proteínas de sinalização celular no ambiente tecidual e células migratórias. Como resultado de um vasto conhecimento acumulado em áreas como a fisiologia, farmacologia e biologia molecular, a partir da década de 1980 surge uma visão mais abrangente do processo inflamatório, passando a reconhecê-lo como decorrente de uma complexa rede eventos bioquímicos e celulares interconectados, atuando como força motriz associada a várias doenças crônicas, incluindo a obesidade, diabetes, arteriosclerose, câncer e distúrbio...

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Predominant role of innate pro-inflammatory cytokines in vitiligo disease

Cited by 49 publications

References 41 publications

JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model of Down Syndrome

JAK1 Inhibition Blocks Lethal Immune Hypersensitivity in a Mouse Model of Down Syndrome

Decreased levels of interleukin 27 in the serum of vitiligo patients

Pathophysiological Aspects of Inflammation and Drug Design: an Updated Overview

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