ArticleFrontiers in immunology2026
Induction of dysfunctional CD14
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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11 authors.
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Abstract
Introduction: Severe COVID-19 disease is characterised by a state of hyperinflammation. As key producers of inflammatory mediators in blood, altered inflammatory activity of monocytes within some individuals may contribute to adverse disease outcomes. Methods: Analysis of monocyte activity under settings of infection and inflammation can be challenged by activation-induced shedding of monocyte receptors traditionally used to identify monocyte subsets. Here, we utilised alternative, more robust immunophenotyping approaches to investigate the impact of COVID-19 infection on monocyte phenotype and inflammatory status. Results: Immunophenotype analysis of cryopreserved peripheral blood mononuclear cells from unvaccinated, previously COVID-19 naive individuals (median age 43 years, range 21-95, n=42) with a PCR-confirmed acute COVID-19 infection indicated expansion of a novel population of CD14 Discussion: COVID-19 is associated with expansion of a novel subset of monocytes with impaired inflammatory activity that persist for at least 3 months after acute infection. Whether this population is uniquely expanded by COVID-19, and the long term implications of its persistence post-acute disease, remain to be defined.
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