Dendritic cells: The driver of psoriasis

Wang, Ao; Bai, Yuling

doi:10.1111/1346-8138.15184

Cited by 101 publications

(98 citation statements)

References 149 publications

(218 reference statements)

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“…Activated DCs played a pivotal role in psoriasis pathogenesis. They not only initiated the in ammation, but also sustained it [15] . Activated mast cells were elevated in psoriatic plaque and produced IL-17, IL-22 [16] .…”

Section: Discussionmentioning

confidence: 97%

“…In this study, the severity of psoriasis was indicated by Psoriasis Area and Severity Index (PASI). Based on PASI, the severity was classi ed into three levels: mild (0-12), moderate (12)(13)(14)(15)(16)(17)(18) and severe (> 18) ( Table. 1). Among these innate immune cells, proportion of M0 macrophages and resting mast cells showed correlation with disease severity (Figure. 2).…”

Section: Association Between Innate Immune Cells and Clinical Manifesmentioning

confidence: 99%

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Profiles of Innate Immune Cell Infiltration and Related Core Genes in Psoriasis

Gong

Wang

2020

Preprint

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Background: Psoriasis is an inflammatory skin disease with substantial morbidity. Numerous patients with psoriasis experience recurrence after therapy. The underlying mechanism about psoriasis is still not fully understood. Some evidences suggest that innate immunity may play an unexpected and important role in active severe psoriasis. In this work, the deconvolution algorithm CIBERSORT was conducted to identify the infiltration of innate immune cells and related core genes in psoriatic plaque.Results: Datasets from the Gene Expression Omnibus, including 407 psoriasis lesional, 373 non-lesional and 91 normal skin samples, were downloaded for analysis. Considerable differences of the innate immune cell composition were uncovered between psoriatic plaque and control skin. Results revealed that γδ T cells, resting NK cells, M0 macrophages, M1 macrophages, activated dendritic cells and neutrophils were significantly increased in psoriatic skin, while resting mast cells and active NK cells were significantly decreased. Moreover, the proportion of M0 macrophages or resting mast cells was found to be associated with disease severity. Spearman correlation analysis suggests that RORC and S100A12 genes were related to disease severity, while genes including S100A12, CLEC4C, IL-19, AIM2, IL-17F, PPARGC1A, were correlated with biologics treatment response.Conclusions: Collectively, this work displays innate immune status in psoriatic skin, and provides novel clues for clinical decisions and mechanism study.

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Section: Discussionmentioning

confidence: 97%

Section: Association Between Innate Immune Cells and Clinical Manifesmentioning

confidence: 99%

Profiles of Innate Immune Cell Infiltration and Related Core Genes in Psoriasis

Gong

Wang

2020

Preprint

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“…The skin contains a complex network of DCs mainly composed of epidermal Langerhans cells (LCs), bone-marrow-derived dermal conventional DCs (cDCs), pDCs, and inflammatory DCs (iDCs) [ 25 ]. As the prominent cellular source of IFNα, TNFα, IL12, and IL23, DCs play an important role in psoriasis [ 25 ].…”

Section: Pathogenesis Of Psoriasismentioning

confidence: 99%

“…pDCs originate in the bone marrow and migrate to the skin under pathologic conditions [ 25 ]. pDCs recognize viral nucleic acids and produce large amounts of type I IFNs in response to endosomal Toll-like receptors (TLRs), such as TLR7 and 9 [ 26 , 27 , 28 , 29 ].…”

Section: Pathogenesis Of Psoriasismentioning

confidence: 99%

New Treatment Addressing the Pathogenesis of Psoriasis

Tokuyama

Mabuchi

2020

IJMS

190

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Psoriasis is an immune cell-mediated inflammatory skin disease. The interleukin (IL)23/IL17 axis plays an important role in the development of psoriasis. The effectiveness of biologic treatments such as tumor necrosis factor (TNF)α inhibitors (infliximab, adalimumab, certolizumab pegol), IL23 inhibitors (ustekinumab, guselkumab, tildrakizumab, risankizumab), and IL17 inhibitors (secukinumab, ixekizumab, brodalumab) have verified these findings. Immune-related cells such as dendritic cells (DCs) and macrophages, in addition to Toll-like receptors and cytokines such as interferon (IFN)α, TNFα, IFNɤ, IL12, IL22, IL23, and IL17, are related to the pathogenesis of psoriasis. Here, we first review new insights regarding the pathogenesis of psoriasis, as it relates to DCs, Langerhans cells, macrophages, the signal transducer and activator of transcription 3 pathway, and aryl hydrocarbon receptor in cutaneous vascular endothelial cells. Based on these findings, we summarize currently available oral treatments and biologics. Furthermore, we describe a new treatment option including Janus kinase inhibitor, tyrosine kinase 2 inhibitor, modulator of sphingosine 1-phosphate receptor 1, and Rho-associated kinase 2 inhibitor.

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“…The current model of psoriasis pathogenesis considers that it is the crosstalk between the complex network of skin DCs, T cells (mainly Th17 [87]) and resident KCs that generate inflammatory and immune routes which are responsible for the initiation, progression and persistence of the disease [73,85,88]. Thus, psoriasis seems to arise in genetically predisposed individuals with an abnormal innate and adaptive immune response to environmental factors that results in a hyperproliferation of KCs, but the exact mechanisms behind these are not completely understood [89,90].…”

Section: The Pathogenesis Of Psoriasismentioning

confidence: 99%

The Brain–Skin Connection and the Pathogenesis of Psoriasis: A Review with a Focus on the Serotonergic System

Martins¹,

Ascenso²,

Ribeiro³

et al. 2020

Cells

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Psoriasis is a common non-communicable chronic immune-mediated skin disease, affecting approximately 125 million people in the world. Its pathogenesis results from a combination of genetic and environmental factors. The pathogenesis of psoriasis seems to be driven by the interaction between innate immune cells, adaptive immune cells and keratinocytes, in a process mediated by cytokines (including interleukins (IL)-6, IL-17 and IL-22, interferon and tumor necrosis factor) and other signaling molecules. This leads to an inflammatory process with increased proliferation of epidermal cells, neo-angiogenesis and infiltration of dendritic cells in the skin. Dysfunctional de novo glucocorticoid synthesis in psoriatic keratinocytes and the skin microbiome have also been suggested as mediators in the pathogenesis of this disease. To understand psoriasis, it is essential to comprehend the processes underlying the skin immunity and neuroendocrinology. This review paper focuses on the skin as a neuroendocrine organ and summarizes what is known about the skin immune system, the brain–skin connection and the role played by the serotonergic system in skin. Subsequently, the alterations of neuroimmune processes and of the serotonergic system in psoriatic skin are discussed, as well as, briefly, the genetic basis of psoriasis.

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Dendritic cells: The driver of psoriasis

Cited by 101 publications

References 149 publications

Profiles of Innate Immune Cell Infiltration and Related Core Genes in Psoriasis

Profiles of Innate Immune Cell Infiltration and Related Core Genes in Psoriasis

New Treatment Addressing the Pathogenesis of Psoriasis

The Brain–Skin Connection and the Pathogenesis of Psoriasis: A Review with a Focus on the Serotonergic System

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