The IL-23/IL-17 Pathway in Inflammatory Skin Diseases: From Bench to Bedside

“…A mouse model, the imiquimod-induced psoriasis model, mimics human psoriasis skin lesions, and has helped develop an understanding of the pathogenesis of psoriasis based on IL-23/IL-17-mediated inflammatory skin lesions [ 15 ]. The IL-17-mediated pathway enhances inflammatory reactions in the epidermis, and keratinocytes produce various inflammatory cytokines, chemokines, and antimicrobial peptides [ 16 ].…”

Section: Pathogenesis Of Inflammatory Skin Diseasesmentioning

confidence: 99%

Daily Lifestyle and Inflammatory Skin Diseases

Sawada

Saito‐Sasaki

Mashima

et al. 2021

IJMS

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Throughout life, it is necessary to adapt to the Earth’s environment in order to survive. A typical example of this is that the daily Earth cycle is different from the circadian rhythm in human beings; however, the ability to adapt to the Earth cycle has contributed to the development of human evolution. In addition, humans can consume and digest Earth-derived foods and use luxury materials for nutrition and enrichment of their lives, as an adaptation to the Earth’s environment. Recent studies have shown that daily lifestyles are closely related to human health; however, less attention has been paid to the fact that obesity due to excessive energy intake, smoking, and alcohol consumption contributes to the development of inflammatory skin diseases. Gluten or wheat protein, smoking and alcohol, sleep disturbance, and obesity drive the helper T (Th)1/Th2/Th17 immune response, whereas dietary fiber and omega-3 fatty acids negatively regulate inflammatory cytokine production. In this review, we have focused on daily lifestyles and the mechanisms involved in the pathogenesis of inflammatory skin diseases.

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“…Furthermore, most of the infiltrating dermal DCs produce IL-23 to maintain the IL-17-generating T cells. Th17 cytokines, mainly IL-17, IL-21, and IL-22, and Th1 cytokines, TNF-α and IFN-γ, in the inflammatory milieu of psoriatic lesions activate keratinocyte proliferation in the epidermis [ 107 , 108 , 109 , 110 ].…”

Section: Current Model For the Pathogenesis Of Psoriasismentioning

confidence: 99%

Therapeutic Development Based on the Immunopathogenic Mechanisms of Psoriasis

et al. 2021

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Psoriasis, a complex inflammatory autoimmune skin disorder that affects 2–3% of the global population, is thought to be genetically predetermined and induced by environmental and immunological factors. In the past decades, basic and clinical studies have significantly expanded knowledge on the molecular, cellular, and immunological mechanisms underlying the pathogenesis of psoriasis. Based on these pathogenic mechanisms, the current disease model emphasizes the role of aberrant Th1 and Th17 responses. Th1 and Th17 immune responses are regulated by a complex network of different cytokines, including TNF-α, IL-17, and IL-23; signal transduction pathways downstream to the cytokine receptors; and various activated transcription factors, including NF-κB, interferon regulatory factors (IRFs), and signal transducer and activator of transcriptions (STATs). The biologics developed to specifically target the cytokines have achieved a better efficacy and safety for the systemic management of psoriasis compared with traditional treatments. Nevertheless, the current therapeutics can only alleviate the symptoms; there is still no cure for psoriasis. Therefore, the development of more effective, safe, and affordable therapeutics for psoriasis is important. In this review, we discussed the current trend of therapeutic development for psoriasis based on the recent discoveries in the immune modulation of the inflammatory response in psoriasis.

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The IL-23/IL-17 Pathway in Inflammatory Skin Diseases: From Bench to Bedside

Cited by 196 publications

References 172 publications

Psoriasis: Comorbidities

Psoriasis: Comorbidities

Daily Lifestyle and Inflammatory Skin Diseases

Therapeutic Development Based on the Immunopathogenic Mechanisms of Psoriasis

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