ArticleScientific reports2026
Regulatory effects of beta-2-microglobulin on reactive oxygen species generation in polymorphonuclear cells.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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.
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Who cites it
1 citing paper in PubMed.
- Construction of a prediction model for retinopathy of prematurity based on placenta-derived genes and clinical variables.Translational pediatrics · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta-2-microglobulin (β2m) constitutes the invariant light chain of the major histocompatibility complex class I (MHC I) and is therefore expressed on all nucleated cells. Soluble β2m is present in biological fluids, platelets and neutrophil granules. Immune and epithelial cells can upregulate the production and secretion of β2m in response to pro-inflammatory cytokines. In the present study, we investigated the effects of exogenous β2m and two proteolytically processed forms, cK58β2m and dK58β2m, on reactive oxygen species (ROS) production in polymorphonuclear leukocytes (PMNs). β2m was shown to enhance ROS generation triggered by latex beads, while cK58β2m and dK58β2m suppressed both baseline ROS levels and responses to latex beads, TNF-α, and fMLF. The inhibitory effect of cK58β2m and dK58β2m was also confirmed in DMSO-differentiated HL-60 cells, a neutrophil-like cell line. Furthermore, treatment with dK58β2m impaired the recruitment of p47phox and p67phox to the plasma membrane following fMLF stimulation, two key subunits of the NADPH oxidase complex responsible for superoxide anion production in neutrophils. This may explain the reduced ROS production observed in cells treated with dK58β2m. These results highlight a potential role for β2m, cK58β2m, and dK58β2m in modulating the innate immune response through control of ROS production in PMNs.
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