In one paragraphArticle in Nature communications, 2025. 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
5 · Who and what moneyAuthors and funding
18 authors.
Thinh-Phat Cao *Infection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.ORCID http://orcid.org/0000-0001-9387-5460 Guan-Ru Liao *Infection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.
Tan-Yun ChengDivision of Rheumatology, Immunity and Inflammation, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Yanqiong ChenInfection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.
Laura CiacchiInfection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.ORCID http://orcid.org/0000-0002-9708-1526 Thomas S FulfordDepartment of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity at the University of Melbourne, Melbourne, Parkville, VIC, Australia.ORCID http://orcid.org/0000-0002-7210-5739 Rachel FarquharInfection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.
Jade KollmorgenInfection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.
Adam P UldrichDepartment of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity at the University of Melbourne, Melbourne, Parkville, VIC, Australia.ORCID http://orcid.org/0000-0002-6350-5976 Dale I GodfreyDepartment of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity at the University of Melbourne, Melbourne, Parkville, VIC, Australia.ORCID http://orcid.org/0000-0002-3009-5472 Nicholas A GherardinDepartment of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity at the University of Melbourne, Melbourne, Parkville, VIC, Australia.ORCID http://orcid.org/0000-0003-4690-2571 D Branch MoodyDivision of Rheumatology, Immunity and Inflammation, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. bmoody@bwh.harvard.edu.
Adam ShahineInfection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia. adam.shahine@monash.edu.ORCID http://orcid.org/0000-0001-7717-4437 Jamie RossjohnInfection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia. Jamie.rossjohn@monash.edu.ORCID http://orcid.org/0000-0002-2020-7522 Funding
Study of M. tuberculosis under human host selection to identify virulence and barrier lipids (Project 1)U19AI162584 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI WOOD, ROBIN · 2021 to 2025
$13.5MT cell response to CDI-restricted lipids in tuberculosisR01AI049313 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI MOODY, DAVID BRANCH · 2001 to 2025
$10.6MCD1 Presentation of Self Lipids to Human T CellsR01AR048632 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI MOODY, DAVID BRANCH · 2002 to 2024
$9.4MCD1 autoreactive T cells in human inflammatory skin diseaseR37AR048632 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI DAVID Branch MOODY · 2025 to 2026
$1.1MNIAID NIH HHS R01 AI049313NIAID NIH HHS U19 AI162584NIAMS NIH HHS R01 AR048632NIAMS NIH HHS R37 AR048632Wellcome Trust
6 · The paper itselfAbstract
For the MHC, MR1 and CD1 systems, antigen recognition involves contact of the membrane distal surfaces of both the αβ T cell receptor (TCR) and the antigen-presenting molecule. Whether other antigen display mechanisms by antigen-presenting molecules operate remains unknown. Here, we report mass spectrometry analyses of endogenous lipids captured by CD1c when bound to an autoreactive αβ TCR. CD1c binds twenty-six lipid species with bulky headgroups that cannot fit within the tight TCR-CD1c interface. We determined the crystal structures of CD1c presenting several gangliosides, revealing a general mechanism whereby two lipids, rather than one, are bound in the CD1c cleft. Bulky lipids are oriented sideways so that their polar headgroups protrude laterally through a side portal of the CD1c molecule - an evolutionarily conserved structural feature. The sideways-presented ganglioside headgroups do not hinder TCR binding and so represent a mechanism that allows autoreactive TCR recognition of CD1c. In addition, ex vivo studies showed that the sideways-presented gangliosides can also represent TCR recognition determinants. These findings reveal that CD1c simultaneously presents two lipid antigens from the top and side of its cleft, a general mechanism that differs markedly from other antigen-presenting molecules.
Indexed as
Antigen PresentationAntigens, CD1LipidsAnimalsCrystallography, X-RayGangliosidesGlycoproteinsHumansModels, MolecularProtein BindingReceptors, Antigen, T-Cell, alpha-betaAntigens, CD1CD1C protein, humanGangliosidesGlycoproteinsLipidsReceptors, Antigen, T-Cell, alpha-beta
Identifiers
PMID41476042
PMCPMC12847783
What OpenQuestion holds
Textmetadata
LicenceCC BY-NC-ND
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