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Molecular Mechanism and Therapy of Psoriasis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 741

Special Issue Editor


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Guest Editor
Department of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan
Interests: psoriasis; inflammatory skin disease; cytokine; ILC3, biologics; JAK inhibitor; small molecule
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Special Issue Information

Dear Colleagues,

The skin is one of the largest immune organs involving innate and acquired immune systems. Thus, it can respond to exogenous stimuli, producing large amounts of proinflammatory cytokines that result in systemic inflammation.

Psoriasis is an intractable inflammatory cytokine-mediated skin disorder. Due to complications and comorbidities, including cerebro-cardiovascular complications, the average life span of people with psoriasis is 6 years shorter than that of the population without a history of psoriasis. Numerous types of biologics and small molecules have been discovered and used in routine clinical practice. They have proven to be remarkably effective and have improved patients’ quality of life. However, there are still many unanswered questions regarding the pathogenesis of the disease, and further discoveries of new cytokines and mediators are expected.

For this Special Issue, we welcome clinical evidence and research findings focusing on molecular mechanisms and therapy in psoriasis.

Prof. Dr. Keiichi Yamanaka
Guest Editor

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Keywords

  • psoriasis
  • inflammatory skin disease
  • cytokine
  • innate lymphoid cell
  • systemic inflammation
  • JAK inhibitor
  • small molecule

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Published Papers (1 paper)

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Research

16 pages, 8635 KiB  
Article
Amelioration of Systemic Amyloidosis by Blocking IL-17A and Not by IL-17F, and Arteriosclerosis by Blocking Both IL-17A and IL-17F in an Inflammatory Skin Mouse Model
by Takehisa Nakanishi, Shohei Iida, Masako Ichishi, Makoto Kondo, Mai Nishimura, Ayaka Ichikawa, Yoshiaki Matsushima, Yoichiro Iwakura, Masatoshi Watanabe and Keiichi Yamanaka
Int. J. Mol. Sci. 2024, 25(21), 11617; https://doi.org/10.3390/ijms252111617 - 29 Oct 2024
Viewed by 576
Abstract
There are comorbidities and complications in atopic dermatitis and psoriasis that often occur after the appearance of skin inflammation. Statistically, data show that patients with psoriasis and atopic dermatitis have a shorter life expectancy than patients without psoriatic dermatitis, due to the occurrence [...] Read more.
There are comorbidities and complications in atopic dermatitis and psoriasis that often occur after the appearance of skin inflammation. Statistically, data show that patients with psoriasis and atopic dermatitis have a shorter life expectancy than patients without psoriatic dermatitis, due to the occurrence of arteriosclerosis, myocardial infarction, and cerebral infarction. Many types of skin inflammation are treated with various antibody preparations, and marked improvement in patients’ quality of life can be achieved. The next theme is to understand the pathogenesis of arteriosclerosis, myocardial infarction, stroke, and other complications associated with dermatitis and to find treatments and drugs to reduce their occurrence. The skin, a crucial immune organ, generates large amounts of inflammatory cytokines in response to various stimuli, leading to systemic inflammation and potential damage to internal organs. The link between inflammatory skin conditions like psoriasis and atopic dermatitis with serious health complications such as vascular disorders and systemic amyloidosis has been increasingly recognized. In psoriasis, biological treatments targeting Interleukin (IL)-17A, a key cytokine, have shown promise in reducing cardiovascular risks. Recent developments include treatments that target both IL-17A and IL-17F in the psoriasis field, though each cytokine’s impact on internal organ damage is still under debate. Among visceral complications secondary to dermatitis, systemic amyloidosis and atherosclerosis have been reported to be controlled by suppressing IL-17 in the early stages of dermatitis. Still, it remains unclear whether suppressing IL-17 prevents organ damage in the late stages of persistent severe dermatitis. A study using a long-lasting dermatitis mouse model that overexpressed human caspase-1 in keratinocytes (Kcasp1Tg) investigated the effects of deleting IL-17A and IL-17F on visceral complications. Cross-mating Kcasp1Tg with IL-17A-, IL-17F-, and IL-17AF-deficient mice assessed the skin and visceral organs histologically, and RT-PCR analysis of aortic sclerosis markers was performed. Despite less improvement in dermatitis, deletion of IL-17A in Kcasp1Tg mice showed promising results in reducing multiple organ amyloidosis. On the other hand, the effect was observed in both IL-17A and IL-17F deleted mice for aortic sclerosis. The inhibition of IL-17A and IL-17F was suggested to reduce the risk of developing comorbidities in internal organs. IL-17A and IL-17F were found to act similarly or produce very different results, depending on the organ. Full article
(This article belongs to the Special Issue Molecular Mechanism and Therapy of Psoriasis)
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