ArticleFrontiers in immunology2026
Peroxisomal ABCD1 deficiency in mice drives Th1 bias through 25-HC-LXR signaling in CD4
Reina Maeda, Mayu Oishi, Ryutaro Nagamori, Mari Hikosaka-Kuniishi, Shiro Watanabe, Jung-Bum Lee, Masashi Morita, Takanori So
Abstract read
In one paragraphArticle 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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0citing papers in PubMed
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What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registryThe 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
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4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
8 authors.
Reina MaedaLaboratory of Molecular Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Mayu OishiLaboratory of Molecular Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Ryutaro NagamoriLaboratory of Molecular Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Mari Hikosaka-KuniishiLaboratory of Molecular Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Shiro WatanabeDepartment of Technical Assistance, Research Promotion Organization, University of Toyama, Toyama, Japan.
Jung-Bum LeeLaboratory of Plant Resource Sciences, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Masashi MoritaLaboratory of Molecular Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Takanori SoLaboratory of Molecular Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
X-linked adrenoleukodystrophy (X-ALD) is driven by ABCD1 dysfunction, causing very-long-chain fatty acid (VLCFA) accumulation and cerebral inflammation, yet the role of T cells in X-ALD remains unclear. Here, we show that
Indexed as
AdrenoleukodystrophyATP Binding Cassette Transporter, Subfamily D, Member 1CD4-Positive T-LymphocytesHydroxycholesterolsLiver X ReceptorsPeroxisomesSignal TransductionTh1 CellsAnimalsFluorocarbonsHydrocarbons, FluorinatedMiceMice, Inbred C57BLMice, KnockoutPositive Regulatory Domain I-Binding Factor 1T-Box Domain ProteinsAbcd1 protein, mouseATP Binding Cassette Transporter, Subfamily D, Member 1FluorocarbonsHydrocarbons, FluorinatedHydroxycholesterolsLiver X ReceptorsPositive Regulatory Domain I-Binding Factor 1T-Box Domain Proteins25-hydroxycholesterolABCD1Blimp-1CD4+ T cellLXRperoxisomeX-linked adrenoleukodystrophy
Identifiers
PMID42245638
PMCPMC13230122
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