ArticleVirus research2025
D-dimer drives immune dysregulation in COVID-19 via chemokine modulation and inflammatory signaling.
Article in Virus research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Elevated D-dimer is independently associated with in-hospital mortality in patients withFrontiers in cellular and infection microbiology · 2026Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundd-dimer, a fibrin degradation product and established marker of thrombosis, has been strongly associated with disease severity and poor prognosis in COVID-19. However, its role in immune modulation remains underexplored.
methodsIn this study, we enrolled 356 participants from Shanghai, including patients with mild and severe COVID-19 and SARS-CoV-2-negative controls. Clinical data were collected to assess correlations between d-dimer and immune-related markers. Public transcriptomic datasets, single-cell RNA sequencing (scRNA-seq), and in vitro stimulation of THP-1 cells with clinically relevant d-dimer concentrations were used to investigate d-dimer-associated immune responses.
resultsd-dimer levels were significantly elevated in severe COVID-19 patients and positively correlated with IL-6 and troponin I, while negatively associated with glomerular filtration rate. Integrated transcriptomic and protein interaction analyses identified IL-6 as a central hub in immune-related gene networks. scRNA-seq revealed tissue- and cell-specific IL-6 expression, predominantly in monocytes and T cells. In vitrod-dimer stimulation did not induce IL-6 expression in THP-1 cells but upregulated chemokines (e.g., CXCL5, CXCL6), and enriched key inflammatory pathways, including IL-17 and PI3K-Akt signaling.
conclusionThese findings suggest that d-dimer may modulate the immune microenvironment by influencing chemokine-mediated cell recruitment, contributing to immune dysregulation in severe COVID-19. d-dimer functions not only as a clinical biomarker but also as a potential driver of thromboinflammatory responses.
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