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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
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We are analyzing https://link.springer.com/article/10.1007/s12016-024-08991-7.

Title:
The Immunology of Psoriasis—Current Concepts in Pathogenesis | Clinical Reviews in Allergy & Immunology
Description:
Psoriasis is one of the most common inflammatory skin diseases with a chronic, relapsing-remitting course. The last decades of intense research uncovered a pathological network of interactions between immune cells and other types of cells in the pathogenesis of psoriasis. Emerging evidence indicates that dendritic cells, TH17 cells, and keratinocytes constitute a pathogenic triad in psoriasis. Dendritic cells produce TNF-α and IL-23 to promote T cell differentiation toward TH17 cells that produce key psoriatic cytokines IL-17, IFN-γ, and IL-22. Their activity results in skin inflammation and activation and hyperproliferation of keratinocytes. In addition, other cells and signaling pathways are implicated in the pathogenesis of psoriasis, including TH9 cells, TH22 cells, CD8+ cytotoxic cells, neutrophils, γΓ T cells, and cytokines and chemokines secreted by them. New insights from high-throughput analysis of lesional skin identified novel signaling pathways and cell populations involved in the pathogenesis. These studies not only expanded our knowledge about the mechanisms of immune response and the pathogenesis of psoriasis but also resulted in a revolution in the clinical management of patients with psoriasis. Thus, understanding the mechanisms of immune response in psoriatic inflammation is crucial for further studies, the development of novel therapeutic strategies, and the clinical management of psoriasis patients. The aim of the review was to comprehensively present the dysregulation of immune response in psoriasis with an emphasis on recent findings. Here, we described the role of immune cells, including T cells, B cells, dendritic cells, neutrophils, monocytes, mast cells, and innate lymphoid cells (ILCs), as well as non-immune cells, including keratinocytes, fibroblasts, endothelial cells, and platelets in the initiation, development, and progression of psoriasis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Science
  • Education
  • Health & Fitness

Content Management System {šŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {šŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {šŸ’ø}

We're unsure if the website is profiting.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {šŸ”}

cells, pubmed, psoriasis, article, google, scholar, cas, skin, psoriatic, central, dermatol, immunol, inflammation, immune, role, patients, kcs, cell, expression, response, including, lesions, cytokines, inflammatory, invest, keratinocytes, human, production, dcs, interleukin, increased, disease, ifnγ, neutrophils, lesional, activated, wang, produce, cytokine, pathogenesis, ila, clin, dendritic, activation, nat, sci, proinflammatory, epidermal, memory, tnfα,

Topics {āœ’ļø}

ccr7+/l-selectin+ central memory dual-secreting il-17a/il-22 th17 raf i-mek-erk pathway granulocyte-macrophage colony-stimulating factor tlr4/il-36r-mediated mechanisms [156 il-36-mediated dc-keratinocyte crosstalk ccr7+/l-selectināˆ’ migratory memory il-1β-il-1r signaling pathway simultaneously increases il-17a+ γΓ myeloid-derived suppressor cells article download pdf tumor necrosis factor-alpha de jesĆŗs-gil skin-resident il-17a-producing promotes il-17a-producing γΓ multiple b-cell subsets t-cell profiles cd73/ampk/mtor pathway psoriasis-specific il-17-producing αβ single-cell immune profiling ifn-γ-producing th1 cells cells express il-23r single-cell transcriptomics applied hair follicle-derived il-7 cell-dominated adaptive inflammation cd1d-dependent ifn-gamma production cell–mediated skin inflammation cell-mediated skin inflammation ifn-α completely prevented interleukin-25-mediated autoregulatory circuit unique il-17a signaling human tissue-resident memory single-cell rna sequencing tissue-specific epidermal localization il-17 receptor–based signaling il-17a-producing cd8+ il-17a-producing cd8 tissue-resident memory cd8+ weng teng kw il-17a-producing population anti-il-17a therapeutics [243] il-17f+ ifn-γ+ cells enhanced nf-Īŗb signaling cd3-cd4+ cell subset human skin-homing memory nonprofessional antigen-presenting cells injury-amplified psoriatic inflammation il-17a-producing γΓ full size image ccl27-ccr10 interactions regulate

Questions {ā“}

  • Benhadou F, Mintoff D, Del Marmol V (2019) Psoriasis: keratinocytes or immune cells - which is the trigger?
  • Harvima IT, Nilsson G, Suttle MM, Naukkarinen A (2008) Is there a role for mast cells in psoriasis?

Schema {šŸ—ŗļø}

WebPage:
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         headline:The Immunology of Psoriasis—Current Concepts in Pathogenesis
         description:Psoriasis is one of the most common inflammatory skin diseases with a chronic, relapsing-remitting course. The last decades of intense research uncovered a pathological network of interactions between immune cells and other types of cells in the pathogenesis of psoriasis. Emerging evidence indicates that dendritic cells, TH17 cells, and keratinocytes constitute a pathogenic triad in psoriasis. Dendritic cells produce TNF-α and IL-23 to promote T cell differentiation toward TH17 cells that produce key psoriatic cytokines IL-17, IFN-γ, and IL-22. Their activity results in skin inflammation and activation and hyperproliferation of keratinocytes. In addition, other cells and signaling pathways are implicated in the pathogenesis of psoriasis, including TH9 cells, TH22 cells, CD8+ cytotoxic cells, neutrophils, γΓ T cells, and cytokines and chemokines secreted by them. New insights from high-throughput analysis of lesional skin identified novel signaling pathways and cell populations involved in the pathogenesis. These studies not only expanded our knowledge about the mechanisms of immune response and the pathogenesis of psoriasis but also resulted in a revolution in the clinical management of patients with psoriasis. Thus, understanding the mechanisms of immune response in psoriatic inflammation is crucial for further studies, the development of novel therapeutic strategies, and the clinical management of psoriasis patients. The aim of the review was to comprehensively present the dysregulation of immune response in psoriasis with an emphasis on recent findings. Here, we described the role of immune cells, including T cells, B cells, dendritic cells, neutrophils, monocytes, mast cells, and innate lymphoid cells (ILCs), as well as non-immune cells, including keratinocytes, fibroblasts, endothelial cells, and platelets in the initiation, development, and progression of psoriasis.
         datePublished:2024-04-20T00:00:00Z
         dateModified:2024-04-20T00:00:00Z
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            Internal Medicine
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      headline:The Immunology of Psoriasis—Current Concepts in Pathogenesis
      description:Psoriasis is one of the most common inflammatory skin diseases with a chronic, relapsing-remitting course. The last decades of intense research uncovered a pathological network of interactions between immune cells and other types of cells in the pathogenesis of psoriasis. Emerging evidence indicates that dendritic cells, TH17 cells, and keratinocytes constitute a pathogenic triad in psoriasis. Dendritic cells produce TNF-α and IL-23 to promote T cell differentiation toward TH17 cells that produce key psoriatic cytokines IL-17, IFN-γ, and IL-22. Their activity results in skin inflammation and activation and hyperproliferation of keratinocytes. In addition, other cells and signaling pathways are implicated in the pathogenesis of psoriasis, including TH9 cells, TH22 cells, CD8+ cytotoxic cells, neutrophils, γΓ T cells, and cytokines and chemokines secreted by them. New insights from high-throughput analysis of lesional skin identified novel signaling pathways and cell populations involved in the pathogenesis. These studies not only expanded our knowledge about the mechanisms of immune response and the pathogenesis of psoriasis but also resulted in a revolution in the clinical management of patients with psoriasis. Thus, understanding the mechanisms of immune response in psoriatic inflammation is crucial for further studies, the development of novel therapeutic strategies, and the clinical management of psoriasis patients. The aim of the review was to comprehensively present the dysregulation of immune response in psoriasis with an emphasis on recent findings. Here, we described the role of immune cells, including T cells, B cells, dendritic cells, neutrophils, monocytes, mast cells, and innate lymphoid cells (ILCs), as well as non-immune cells, including keratinocytes, fibroblasts, endothelial cells, and platelets in the initiation, development, and progression of psoriasis.
      datePublished:2024-04-20T00:00:00Z
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         Immune response
         Skin inflammation
         TH17 cells
         Keratinocyte
         Allergology
         Immunology
         Internal Medicine
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         name:Laboratory of Immunology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland
         type:PostalAddress
      name:Medical University of Warsaw
      address:
         name:Department of Methodology, Medical University of Warsaw, Warsaw, Poland
         type:PostalAddress
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            address:
               name:University Centre of Veterinary Medicine, University of Agriculture in Krakow, Krakow, Poland
               type:PostalAddress
            type:Organization
      name:Monika Pieniawska
      affiliation:
            name:Polish Academy of Sciences
            address:
               name:Institute of Human Genetics, Polish Academy of Sciences, Poznań, Poland
               type:PostalAddress
            type:Organization
      name:Tomasz M. Grzywa
      affiliation:
            name:Mossakowski Medical Research Institute, Polish Academy of Sciences
            address:
               name:Laboratory of Immunology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland
               type:PostalAddress
            type:Organization
            name:Medical University of Warsaw
            address:
               name:Department of Methodology, Medical University of Warsaw, Warsaw, Poland
               type:PostalAddress
            type:Organization
            name:Children’s Hospital of Philadelphia
            address:
               name:The Raymond G. Perelman Center for Cellular and Molecular Therapeutics, Department of Pathology and Laboratory Medicine, Children’s Hospital of Philadelphia, Philadelphia, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
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      name:University Centre of Veterinary Medicine, University of Agriculture in Krakow, Krakow, Poland
      name:Institute of Human Genetics, Polish Academy of Sciences, Poznań, Poland
      name:Laboratory of Immunology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland
      name:Department of Methodology, Medical University of Warsaw, Warsaw, Poland
      name:The Raymond G. Perelman Center for Cellular and Molecular Therapeutics, Department of Pathology and Laboratory Medicine, Children’s Hospital of Philadelphia, Philadelphia, USA

External Links {šŸ”—}(1064)

Analytics and Tracking {šŸ“Š}

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Libraries {šŸ“š}

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6.53s.