ArticleInflammation2013
Proliferation and apoptosis of peripheral blood mononuclear cells in patients with oral lichen planus.
Article in Inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Probiotics as Potential Biological Immunomodulators in the Management of Oral Lichen Planus: What's New?International journal of molecular sciences · 2022Review
- Suppression of gelatinase activity in human peripheral blood mononuclear cells by verapamil.Cell journal · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral lichen planus (OLP) is generally accepted to be a T cell-mediated chronic inflammatory disease with an unclear pathogenesis. There have been numerous studies on the proliferation and apoptosis of T cells in situ. In contrast, research on the proliferation and apoptosis of peripheral blood mononuclear cells (PBMCs) in patients with OLP is rare. The aim of the present study was to investigate the proliferation and apoptosis of PBMCs in patients with OLP. PBMCs were isolated from 20 patients with reticular OLP, 20 patients with atrophic-erosive OLP, and 20 healthy volunteers. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl-2,5-tetrazolium bromide assays were performed to investigate the proliferation of PBMCs, and caspase-3 colorimetric assays were performed to investigate the apoptosis of PBMCs. The proliferation rate of PBMCs in atrophic-erosive OLP subjects was significantly higher than that in both healthy (P < 0.05) and reticular OLP (P < 0.05) subjects. In contrast, the proliferation rate of PBMCs in reticular OLP subjects was significantly lower than that in healthy subjects (P < 0.05). The apoptosis rates of PBMCs in OLP subjects (P < 0.05) and atrophic-erosive OLP subjects (P < 0.05) were significantly lower than the apoptosis rate in the healthy group. Our findings reinforce the view that T cell-mediated immune responses play a critical role in the pathogenesis of OLP. It can reasonably be concluded that these abnormalities are linked to the presence of inflammatory infiltrates.
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Registered trials
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