ArticlePloS one2015
Deletion of IL-18 Expression Ameliorates Spontaneous Kidney Failure in MRLlpr Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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
8 citing papers in PubMed, 15 citations in OpenAlex.
- Evaluation of causal associations between interleukin-18 levels and immune-mediated inflammatory diseases: a Mendelian randomization study.BMC medical genomics · 2023Article
- Th1-related transcription factors and cytokines in systemic lupus erythematosus.Frontiers in immunology · 2023Review
- IL-18 deficiency ameliorates the progression from AKI to CKD.Cell death & disease · 2022Article
- Review
- Interleukin-18 in Inflammatory Kidney Disease.Frontiers in medicine · 2021Review
- Reporting animal research: Explanation and elaboration for the ARRIVE guidelines 2.0.PLoS biology · 2020Article
- Analysis of Serum Interleukin (IL)-1β and IL-18 in Systemic Lupus Erythematosus.Frontiers in immunology · 2018Article
- Control of lupus nephritis by changes of gut microbiota.Microbiome · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of IL-18 in the pathogenesis of systemic lupus erythematosus is still not definitively solved. In this study, we generated MRLlpr mice, which develop a disease resembling systemic lupus erythematosus, genetically devoid of IL-18 expression. These mice in comparison to IL-18-competent MRLlpr mice show reduced signs of renal pathogenesis, while other parameters such as mean survival time, lymphadenopathy, constitutive interferon-γ production, and frequency of CD3+B220+ abnormal T cells were without differences. We conclude that in the systemic lupus erythematosus syndrom IL-18 is involved specifically in the renal pathogenesis.
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Registered trials
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