ArticleThe American journal of pathology2017
Tumor Necrosis Factor-α and IL-17A Activation Induces Pericyte-Mediated Basement Membrane Remodeling in Human Neutrophilic Dermatoses.
Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Molecular Characteristics of Sweet Syndrome: A Systematic Review.Experimental dermatology · 2024Pooled it
- Regulation of neutrophil function by the extracellular matrix.Biochemical Society transactions · 2025Review
- Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025Review
- Engineered microvascular basement membrane mimetic for real-time neutrophil tracking in the microvascular wall.Bioengineering & translational medicine · 2025Article
- Treatment with cyclosporine attenuates the inflammatory process and severity of bisphosphonate-induced osteonecrosis of the jaws in rats.Inflammopharmacology · 2025Article
- TGF-β1 Drives Integrin-Dependent Pericyte Migration and Microvascular Destabilization in Fibrotic Disease.The American journal of pathology · 2024Article
- The Role of Pericytes in Regulation of Innate and Adaptive Immunity.Biomedicines · 2023Review
- Interleukin-17 plays a role in dental pulp inflammation mediated by zoledronic acid: a mechanism unrelated to the Th17 immune response?Journal of applied oral science : revista FOB · 2023Article
- IL-17A Damages the Blood-Retinal Barrier through Activating the Janus Kinase 1 Pathway.Biomedicines · 2021Article
- Review
- T helper 17 cells in the pathophysiology of acute and chronic kidney disease.Kidney research and clinical practice · 2021Article
- Microphysiological Systems for Studying Cellular Crosstalk During the Neutrophil Response to Infection.Frontiers in immunology · 2021Review
- A subtype of cerebrovascular pericytes is associated with blood-brain barrier disruption that develops during normal aging and simian immunodeficiency virus infection.Neurobiology of aging · 2020Article
- The distribution of immune cells within combined hepatocellular carcinoma and cholangiocarcinoma predicts clinical outcome.Clinical and translational medicine · 2020Article
- Minimally Invasive Delivery of Microbeads with Encapsulated, Viable and Quiescent Neural Stem Cells to the Adult Subventricular Zone.Scientific reports · 2019Article
- Matrix Metalloproteinase-3 is Key Effector of TNF-α-Induced Collagen Degradation in Skin.International journal of molecular sciences · 2019Article
- Inhibition of NET-1 suppresses proliferation and promotes apoptosis of hepatocellular carcinoma cells by activating the PI3K/AKT signaling pathway.Experimental and therapeutic medicine · 2019Article
- Thalidomide in the Treatment of Sweet's Syndrome and Eosinophilic Folliculitis Associated With Immune Reconstitution Inflammatory Syndrome.Frontiers in medicine · 2019Article
- Insights Into the Pathogenesis of Sweet's Syndrome.Frontiers in immunology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Sweet syndrome (SS) is a prototypical neutrophilic dermatosis, a class of inflammatory diseases marked by elevated levels of tumor necrosis factor (TNF)-α and IL-17A, pathologic neutrophil recruitment, and microvascular remodeling. Histologic analyses of four matrix proteins-collagen I and IV, laminin, and fibronectin-in skin biopsies of patients with SS reveal that the basement membrane of dermal postcapillary venules undergoes changes in structure and composition. Increased neutrophil recruitment in vivo was associated with increases in collagen IV, decreases in laminin, and varied changes in fibronectin. In vitro studies using TNF-α and IL-17A were conducted to dissect basement membrane remodeling. Prolonged dual activation of cultured human pericytes with TNF-α and IL-17A augmented collagen IV production, similar to in vivo remodeling. Co-activation of pericytes with TNF-α and IL-17A also elevated fibronectin levels with little direct effect on laminin. However, the expression of fibronectin- and laminin-specific matrix metalloproteinases (MMPs), particularly MMP-3, was significantly up-regulated. Interactions between pericytes and neutrophils in culture yielded even higher levels of active MMPs, facilitating fibronectin and laminin degradation, and likely contributing to the varied levels of detectable fibronectin and the decreases in laminin observed in vivo. These data indicate that pericyte-neutrophil interactions play a role in mediating microvascular changes in SS and suggest that targeting MMP-3 may be effective in protecting vascular wall integrity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.