Vitiligo melanocytes in long-term culture show normal constitutive and cytokine-induced expression of intercellular adhesion molecule-1 and major histocompatibility complex class I and class II molecules

Hedley, John; Metcalfe,; Gawkrodger, None; Weetman,; Neil, M. Walker

doi:10.1046/j.1365-2133.1998.02550.x

Cited by 26 publications

(21 citation statements)

References 57 publications

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“…Furthermore, IFNG, TNFA and TNFB stimulate the expression of ICAM1 on the cell-surface of melanocytes [23], which is important for activating T-cells and recruiting leukocytes [69], [70]. ICAM1 protein levels are upregulated in vitiligo skin and in melanocytes from perilesional vitiligo skin [71], [24].…”

Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor B (TNFB) Genetic Variants and Its Increased Expression Are Associated with Vitiligo Susceptibility

et al. 2013

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Genetic polymorphisms in TNFB are involved in the regulation of its expression and are found to be associated with various autoimmune diseases. The aim of the present study was to determine whether TNFB +252A/G (rs909253) and exon 3 C/A (rs1041981) polymorphisms are associated with vitiligo susceptibility, and expression of TNFB and ICAM1 affects the disease onset and progression. We have earlier reported the role of TNFA in autoimmune pathogenesis of vitiligo, and we now show the involvement of TNFB in vitiligo pathogenesis. The two polymorphisms investigated in the TNFB were in strong linkage disequilibrium and significantly associated with vitiligo. TNFB and ICAM1 transcripts were significantly increased in patients compared to controls. Active vitiligo patients showed significant increase in TNFB transcripts compared to stable vitiligo. The genotype-phenotype analysis revealed that TNFB expression levels were higher in patients with GG and AA genotypes as compared to controls. Patients with the early age of onset and female patients showed higher TNFB and ICAM1 expression. Overall, our findings suggest that the increased TNFB transcript levels in vitiligo patients could result, at least in part, from variations at the genetic level which in turn leads to increased ICAM1 expression. For the first time, we show that TNFB +252A/G and exon 3 C/A polymorphisms are associated with vitiligo susceptibility and influence the TNFB and ICAM1 expression. Moreover, the study also emphasizes influence of TNFB and ICAM1 on the disease progression, onset and gender bias for developing vitiligo.

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Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor B (TNFB) Genetic Variants and Its Increased Expression Are Associated with Vitiligo Susceptibility

et al. 2013

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“…In fact, IFN‐γ and TNF‐α are observed to promote synergistically the inflammatory response, which is accredited to the cooperative interaction between the transcription factors signal transducer and activator of transcription‐1 and NF‐κB . Furthermore, IFN‐γ, TNF‐α and TNF‐β induced the expression of intercellular adhesion molecule (ICAM)1 on the surface of melanocytes, which promotes leucocyte recruitment and T‐cell activation …”

Section: Reduced Regulatory T‐cell Activity May Contribute To Diseasementioning

confidence: 99%

Tumour necrosis factor-α inhibition can stabilize disease in progressive vitiligo

et al. 2015

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TNF-α, a proinflammatory cytokine central to many autoimmune diseases, has been implicated in the depigmentation process in vitiligo. We reviewed its role in vitiligo by exploring its pro- and anti-inflammatory properties and examined the effects of blocking its actions with TNF-α antagonist therapeutics in reports available in the literature. We found that TNF-α inhibition halts disease progression in patients with progressive vitiligo but that, paradoxically, treatment can be associated with de novo vitiligo development in some patients when used to treat other autoimmune conditions, particularly when using adalimumab and infliximab. These studies reinforce the importance of stating appropriate outcomes measures as most pilot trials proposed to measure repigmentation, whereas halting depigmentation was commonly overlooked as a measure of success. We conclude that TNF inhibition was useful for patients with progressive vitiligo, where TNF-α inhibition is able to quash cytotoxic T cell-mediated melanocyte destruction. However, a lingering concern for initiating de novo disease will likely prevent a more widespread application of TNF inhibitors to treat vitiligo.

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“…Its mRNA expression has increased in vitiligo involved and uninvolved skin compared with control skin [15,29]. IFNG stimulates the expression of intercellular adhesion molecule 1 (ICAM1), which is important for activating T cells and recruiting leukocytes [30,31]. ICAM1 protein expression is upregulated in vitiligo skin and in melanocytes from perilesional vitiligo skin [32].…”

Section: Introductionmentioning

confidence: 98%

The mRNA expression profile of cytokines connected to the regulation of melanocyte functioning in vitiligo skin biopsy samples and peripheral blood mononuclear cells

et al. 2012

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Vitiligo melanocytes in long-term culture show normal constitutive and cytokine-induced expression of intercellular adhesion molecule-1 and major histocompatibility complex class I and class II molecules

Cited by 26 publications

References 57 publications

Tumor Necrosis Factor B (TNFB) Genetic Variants and Its Increased Expression Are Associated with Vitiligo Susceptibility

Tumor Necrosis Factor B (TNFB) Genetic Variants and Its Increased Expression Are Associated with Vitiligo Susceptibility

Tumour necrosis factor-α inhibition can stabilize disease in progressive vitiligo

The mRNA expression profile of cytokines connected to the regulation of melanocyte functioning in vitiligo skin biopsy samples and peripheral blood mononuclear cells

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