Increased serum levels of interleukin‐23 circulating in patients with non‐segmental generalized vitiligo

Vaccaro, Mario; Cannavò, Serafinella Patrizia; Imbesi, S.; Cristani, Mariateresa; Barbuzza, Olga; Tigano, Valeria; Gangemi, Sebastiano

doi:10.1111/ijd.12392

Cited by 31 publications

(25 citation statements)

References 16 publications

(16 reference statements)

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“…147 Serum levels of IL-23 are also elevated in vitiligo. 148 These results supports a notion that common pathogenic pathways or shared autoantigens exist in psoriasis and other autoimmune diseases.…”

Section: Autoimmune Diseases Co-morbid With Psoriasissupporting

confidence: 78%

“…In vitiligo, IFN signature is also involved in the initiation of its immune response with the activation of plasmacytoid DCs . Serum levels of IL‐23 are also elevated in vitiligo . These results supports a notion that common pathogenic pathways or shared autoantigens exist in psoriasis and other autoimmune diseases.…”

Section: Autoimmune Diseases Co‐morbid With Psoriasissupporting

confidence: 63%

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Autoimmunity and autoimmune co‐morbidities in psoriasis

et al. 2018

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SummaryPsoriasis is characterized by widespread scaly erythematous plaques that cause significant physical and psychological burdens for the affected individuals. Accelerated inflammation driven by the tumour necrosis factor-a/ interleukin-23/interleukin-17 axis is now known to be the major mechanism in the development of psoriasis. In addition, psoriasis has an autoimmune nature that manifests as autoreactive T cells and is comorbid with other autoimmune diseases, such as autoimmune bullous diseases, vitiligo, alopecia and thyroiditis. In this article, we review the recent topics on autoimmunity and autoimmune co-morbidities in psoriasis.

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Section: Autoimmune Diseases Co-morbid With Psoriasissupporting

confidence: 78%

Section: Autoimmune Diseases Co‐morbid With Psoriasissupporting

confidence: 63%

Autoimmunity and autoimmune co‐morbidities in psoriasis

et al. 2018

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“…IL-23 was recently established as an important driver of the immune activation in many autoimmune diseases, including psoriasis, rheumatoid arthritis, vitiligo, and IBD [91, 92]. IL-23 induces intracellular pro-inflammatory molecules (JAK2 and Tyk2) in human keratinocytes [93].…”

Section: Th17/il-23 Inhibitionmentioning

confidence: 99%

The Changing Landscape of Alopecia Areata: The Therapeutic Paradigm

Renert‐Yuval

Guttman‐Yassky

2017

Adv Ther

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Alopecia areata (AA), a prevalent inflammatory cause of hair loss, lacks FDA-approved therapeutics for extensive cases, which are associated with very poor rates of spontaneous hair regrowth and major psychological distress. Current treatments for severe cases include broad immune-suppressants, which are associated with significant adverse effects, precluding long-term use, with rapid hair loss following treatment termination. As a result of the extent of the disease in severe cases, topical contact sensitizers and intralesional treatments are of limited use. The pathogenesis of AA is not yet fully understood, but recent investigations of the immune activation in AA skin reveal Th1/IFN-γ, as well as Th2, PDE4, IL-23, and IL-9 upregulations. Tissue analyses of both animal models and human lesions following broad-acting and cytokine-specific therapeutics (such as JAK inhibitors and ustekinumab, respectively) provide another opportunity for important insights into the pathogenesis of AA. As reviewed in this paper, numerous novel therapeutics are undergoing clinical trials for AA, emphasizing the potential transformation of the clinical practice of AA, which is currently lacking. Dermatologists are already familiar with the revolution in disease management of psoriasis, stemming from better understanding of immune dysregulations, and atopic dermatitis will soon follow a similar path. In light of these recent developments, the therapeutic arena of AA treatments is finally getting more exciting. AA will join the lengthening list of dermatologic diseases with mechanism-targeted drugs, thus changing the face of AA.

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“…Abdallah et al (29) reported that IL-6 was the most sensitive serum marker to distinguish active from stable vitiligo. Vaccaro et al (30) reported that IL-23 serum levels were notably higher in patients with vitiligo than controls, and positively correlated with disease duration, disease activity, and the extent of vitiligo. These above studies suggest that Th17 cells participate in the pathogenesis of vitiligo.…”

Section: Discussionmentioning

confidence: 99%

Critical role of metabotropic glutamate receptor 4 in bone marrow-derived dendritic cells in the Th17 cell differentiation and the melanogenesis of B16 cells

Zhao

Zhou

Liu

et al. 2020

Braz J Med Biol Res

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Vitiligo is an acquired pigmentary disorder resulting from selective destruction of melanocytes. Emerging studies have suggested that T helper cell 17 (Th17) is potentially implicated in vitiligo development and progression. It was recently discovered that metabotropic glutamate receptor 4 (mGluR4) can modulate Th17-mediated adaptive immunity. However, the influence of mGluR4 on melanogenesis of melanocytes has yet to be elucidated. In the present study, we primarily cultured mouse bone marrow-derived dendritic cells (BMDC) and then knocked down and over-expressed mGluR4 using transfection. Transduced BMDC were co-cultured with CD4 + T cells and the expression of Th17-related cytokines were measured. The morphology and melanogenesis of B16 cells were observed after being treated with co-culture medium of CD4 + T cells and transduced BMDC. We found that mGluR4 knockdown did not affect the co-stimulatory CD80 and CD86 upregulation after lipopolysaccharide stimulation but did increase the expression of Th17-related cytokines, and further down-regulated the expression of microphthalmia-associated transcription factor (MITF) and the downstream genes, decreased melanin production, and destroyed the morphology of B16 cells. Conversely, over-expression of mGluR4 reduced the expression of CD80 and CD86, suppressed the production of Th17-related cytokines, increased the expression of MITF, and did not destroy the morphology of B16 cells. Our study confirmed that mGluR4 modulated the Th17 cell polarization and resulted in the alteration of melanogenesis and morphology of B16 cells. Collectively, these findings suggest mGluR4 might be a potent target involved in the immune pathogenesis of vitiligo.

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Increased serum levels of interleukin‐23 circulating in patients with non‐segmental generalized vitiligo

Abstract: The inhibition of IL-23 might be a novel strategy in the therapy of autoimmune inflammatory diseases like vitiligo.

Cited by 31 publications

References 16 publications

Autoimmunity and autoimmune co‐morbidities in psoriasis

Autoimmunity and autoimmune co‐morbidities in psoriasis

The Changing Landscape of Alopecia Areata: The Therapeutic Paradigm

Critical role of metabotropic glutamate receptor 4 in bone marrow-derived dendritic cells in the Th17 cell differentiation and the melanogenesis of B16 cells

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