ArticlePloS one2012
CD98 positive eosinophils contribute to T helper 1 pattern inflammation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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
5 citing papers in PubMed, 11 citations in OpenAlex.
- Nano-drug delivery systems (NDDS) in metabolic dysfunction-associated steatotic liver disease (MASLD): current status, prospects and challenges.Frontiers in pharmacology · 2024Review
- siRNA Targeting and Treatment of Gastrointestinal Diseases.Clinical and translational science · 2019Review
- CD98 siRNA-loaded nanoparticles decrease hepatic steatosis in mice.Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2017Article
- Lung-resident eosinophils represent a distinct regulatory eosinophil subset.The Journal of clinical investigation · 2016Article
- Targeting intestinal inflammation with CD98 siRNA/PEI-loaded nanoparticles.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsThe pathogenesis of inflammatory bowel disease (IBD) has not been fully understood yet. Eosinophils (Eo) are one type of the major proinflammatory cells of the chronic inflammation in the intestine. CD98 is involved in the pathogenesis of a number of inflammations. This study aims to elucidate the role of CD98(+) Eos in the initiation of intestinal inflammation.
methodsThe colon biopsies were collected from 60 patients with IBD. The expression of CD98 in the biopsies was examined by immunohistochemistry. The serum levels of the flagellin (FGN) antibody and Eo-derived mediators in the culture supernatants were assessed by enzyme-linked immunosorbent assay. The role of FGN on Eo activation was examined in a cell culture model. The role of FGN in the induction of colitis was observed in a mouse model.
resultsCompared to normal controls, the frequency of CD98(+) Eos was markedly increased in the IBD colon mucosa. FGN were detected in the colon biopsies and in the sera of IBD patients. Exposure to FGN induced the expression of galectin 3 (the ligand of CD98) in dendritic cells. The exposure to galectin 3 activated the CD98(+) Eos. After treatment with FGN intrarectally, mice with eosinophilia showed severe inflammation in the colon.
conclusionsThe interaction of galectin 3 and CD98 can induce Eos to release chemical mediators that contributes to the initiation of the intestinal inflammation.
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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.