Immunohistochemistry of Janus Kinase 1 (JAK1) Expression in Vitiligo

Abdou, Asmaa Gaber; Maraee, Alaa Hassan; Yassien, Hossam; Sarhan, Mona O.

doi:10.4132/jptm.2018.09.18

Cited by 12 publications

(8 citation statements)

References 15 publications

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“…JAK1 expression is much more intense and diffuse in lesional skin from patients with vitiligo compared with healthy tissue. High JAK1 expression is associated with short disease duration and lower percentage of surviving melanocytes 144,145 . All these findings support the investigation of therapies that disrupt the IFN‐γ–CXCR3‐CXCL9/10 axis and the downstream signaling proteins JAK1, JAK2, STAT1 146–148 …”

Section: The Ifn‐γ Receptor Recruits Jak1 and Jak2 Kinasesmentioning

confidence: 59%

Vitiligo: A focus on pathogenesis and its therapeutic implications

Bergqvist

Ezzedine

2021

The Journal of Dermatology

139

106

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Vitiligo is the most common depigmenting disorder affecting 0.1%–2% of the population worldwide. The characteristic white patches result from the selective loss of melanocytes. Sustained recent efforts have resulted in a detailed understanding of the genetic architecture of vitiligo. About 80% of vitiligo risk is attributable to genetic factors; and the rest (20%) is attributable to the environment. Over the past decade, substantial progress has been made in our understanding of the pathogenesis of vitiligo which is now clearly classified as an autoimmune disease. Melanocytes from patients with vitiligo are more susceptible to oxidative stress which begets the release of exosomes and inflammatory cytokines that will lead to activation of the innate immune response and subsequently to adaptive immune response through activation of autoreactive cytotoxic CD8+ T cells. These produce interferon‐γ (IFN‐γ) which promotes disease progression through IFN‐γ‐induced chemokine secretion from surrounding keratinocytes to further recruit T cells to the skin through a positive feedback loop. CD8 tissue‐resident memory T cells are in turn responsible for long‐term maintenance and potential relapse of vitiligo in human patients through cytokine‐mediated recruitment of T cells from the circulation. This review summarizes the current knowledge on vitiligo and attempt to give an overview of the future in vitiligo treatment.

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Section: The Ifn‐γ Receptor Recruits Jak1 and Jak2 Kinasesmentioning

confidence: 59%

Vitiligo: A focus on pathogenesis and its therapeutic implications

Bergqvist

Ezzedine

2021

The Journal of Dermatology

139

106

View full text Add to dashboard Cite

show abstract

“…Lesional skin from patients with vitiligo showed much more intense and diffuse JAK1 expression compared with healthy tissue. Moreover, high JAK1 expression was associated with short disease duration and a lower percentage of surviving melanocytes [113, 114]. These results thereby support investigation of therapies that disrupt the pathway targeting IFN-γ, the IFN-γ receptor, the downstream signaling proteins JAK1, JAK2 and STAT1, and the chemokine CXCL10 and its receptor CXCR3 [115-117].…”

Section: Pathogenesismentioning

confidence: 91%

Vitiligo: A Review

2020

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Vitiligo, a common depigmenting skin disorder, has an estimated prevalence of 0.5-2% of the population worldwide. The disease is characterized by the selective loss of melanocytes which results in typical nonscaly, chalky-white macules. In recent years, considerable progress has been made in our understanding of the pathogenesis of vitiligo which is now clearly classified as an autoimmune disease. Vitiligo is often dismissed as a cosmetic problem, although its effects can be psychologically devastating, often with a considerable burden on daily life. In 2011, an international consensus classified segmental vitiligo separately from all other forms of vitiligo, and the term vitiligo was defined to designate all forms of nonsegmental vitiligo. This review summarizes the current knowledge on vitiligo and attempts to give an overview of the future in vitiligo treatment.

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“…Given the apparent critical role for IFNγ in driving vitiligo inflammation and its downstream signaling dependent on the JAK1-JAK2 heterodimer, it is perhaps not surprising that intense and diffuse JAK1 expression is more present within vitiliginous skin compared with healthy tissue. Moreover, high JAK1 expression was associated with short disease duration and a lower percentage of surviving melanocytes (118, 147, 148).…”

Section: Vitiligomentioning

confidence: 99%

Targeting the Janus Kinase Family in Autoimmune Skin Diseases

2019

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Autoimmune skin diseases are characterized by significant local and systemic inflammation that is largely mediated by the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway. Advanced understanding of this pathway has led to the development of targeted inhibitors of Janus kinases (JAKinibs). As a class, JAK inhibitors effectively treat a multitude of hematologic and inflammatory diseases. Growing evidence suggests that JAK inhibitors are efficacious in atopic dermatitis, alopecia areata, psoriasis, and vitiligo. Additional evidence suggests that JAK inhibition might be broadly useful in dermatology, with early reports of efficacy in several other conditions. JAK inhibitors can be administered orally or used topically and represent a promising new class of medications. Here we review the evolving data on the role of the JAK-STAT pathway in inflammatory dermatoses and the potential therapeutic benefit of JAK-STAT antagonism.

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Immunohistochemistry of Janus Kinase 1 (JAK1) Expression in Vitiligo

Cited by 12 publications

References 15 publications

Vitiligo: A focus on pathogenesis and its therapeutic implications

Vitiligo: A focus on pathogenesis and its therapeutic implications

Vitiligo: A Review

Targeting the Janus Kinase Family in Autoimmune Skin Diseases

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