In one paragraphArticle in The Journal of experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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.
No citing paper in PubMed yet.
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
12 authors.
Angela M ThorntonCellular Immunology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-4175-4154 Xi ChenMolecular and Cellular Immunoregulation Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0009-0005-9675-5276 Wenjia CaoIntegrated Data Sciences Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0009-0008-0808-222X Tovah E MarkowitzIntegrated Data Sciences Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0009-0006-2415-2035 Kimmo VirtanevaGenomic Research Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-5503-1483 Paul A BeareGenomic Research Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-2282-177X Vinay PennaCellular Immunology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-9082-7874 Oksana GavrilovaMouse Metabolism Core, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-9310-1198 Jihyun KimMolecular and Cellular Immunoregulation Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0003-1222-0345 Craig A MartensGenomic Research Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0001-8112-2234 Jinfang ZhuMolecular and Cellular Immunoregulation Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-0117-4745 Ethan M ShevachCellular Immunology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0003-1607-4664 Funding
Studies of the Function of Naturally Occurring and Adaptive T Regulatory CellsZ01AI000959 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHEVACH, ETHAN M. · 2006 to 2008
$5.1MIntramural NIH HHS Z01 AI000959NIH HHS AI000959-20
6 · The paper itselfAbstract
The deletion of the transcription factor Helios in regulatory T cells (Tregs) in mice leads to systemic Th1 immune activation, decreased T follicular regulatory cells, and enhanced germinal center formation. We report here these mice also exhibit acquired lipodystrophy, hepatic steatosis, and insulin resistance. Adipose tissue exhibited lymphocytic infiltration followed by CD8+ T cell-mediated destruction of adipocytes. Helios-deficient Tregs were more frequent in adipose tissue and showed an enhanced effector Treg (eTreg) phenotype (CD62Llo Tcf1lo). The Helios-deficient eTregs in adipose tissue, but not spleen, failed to develop into terminally differentiated eTregs, which express ST2+, CXCR3+, IRF4, or Klrg1+. ChIP-seq studies demonstrated that Helios bound to regulatory elements in multiple genes (Tcf7, Lef1, Bach2, and Id3) known to restrict eTreg generation. Thus, Helios not only directly restricts eTreg generation but also indirectly enforces functional eTreg differentiation. In the absence of Helios, the process of eTreg differentiation proceeds unchecked, resulting in enhanced but dysfunctional eTregs, which fail to control adipose tissue homeostasis.
Indexed as
Adipose TissueAutoimmunityCell DifferentiationDNA-Binding ProteinsT-Lymphocytes, RegulatoryTranscription FactorsAdipocytesAnimalsInsulin ResistanceMiceMice, KnockoutDNA-Binding ProteinsTranscription FactorsZfpn1a2 protein, mouse
Identifiers
PMID42820929
PMCPMC13629518
What Socratic holds
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