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Title:
The Immunology of PsoriasisāCurrent 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.
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Keywords {š}
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 {āļø}
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-selectinā migratory memory il-1β-il-1r signaling pathway simultaneously increases il-17a+āγΓ 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 cellāmediated 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 receptorābased 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?
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headline:The Immunology of PsoriasisāCurrent 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
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Allergology
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headline:The Immunology of PsoriasisāCurrent 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.
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Immune response
Skin inflammation
TH17 cells
Keratinocyte
Allergology
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