Evidence map›Paper›PMID 39472557›Full record

ArticleNature communications2024

Physiological and pathogenic T cell autoreactivity converge in type 1 diabetes.

Anne Eugster, Anna Lorenc, Martin Kotrulev, Yogesh Kamra, Manisha Goel, Katja Steinberg-Bains, Shereen Sabbah, Sevina Dietz, Ezio Bonifacio, Mark Peakman and 1 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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 registry

The 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 literature

Who cites it

17 citing papers in PubMed.

  1. Review
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  5. Donor-derived CD8bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
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  12. Review
  13. Advancements in diabetes research and stem cell therapy: a concise review.Journal of diabetes and metabolic disorders · 2025
    Review
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  15. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Anne Eugster *Technische Universität Dresden, Center for Regenerative Therapies Dresden, Dresden, Germany.ORCID 0000-0001-8009-5959
Anna Lorenc *Department of Immunobiology, Faculty of Life Sciences & Medicine, King's College London, 2nd Floor, Borough Wing, Guy's Hospital, London, UK.ORCID 0000-0002-1406-7607
Martin KotrulevCentre for Research in Molecular Medicine and Chronic Diseases (CiMUS), University of Santiago de Compostela, Santiago de Compostela, Spain.ORCID 0000-0001-8497-3229
Yogesh KamraDepartment of Immunobiology, Faculty of Life Sciences & Medicine, King's College London, 2nd Floor, Borough Wing, Guy's Hospital, London, UK.ORCID 0000-0002-3369-9263
Manisha GoelTechnische Universität Dresden, Center for Regenerative Therapies Dresden, Dresden, Germany.
Katja Steinberg-BainsTechnische Universität Dresden, Center for Regenerative Therapies Dresden, Dresden, Germany.
Shereen SabbahDepartment of Immunobiology, Faculty of Life Sciences & Medicine, King's College London, 2nd Floor, Borough Wing, Guy's Hospital, London, UK.ORCID 0000-0002-0607-5121
Sevina DietzTechnische Universität Dresden, Center for Regenerative Therapies Dresden, Dresden, Germany.ORCID 0000-0001-8360-7868
Ezio BonifacioTechnische Universität Dresden, Center for Regenerative Therapies Dresden, Dresden, Germany.ORCID 0000-0002-8704-4713
Mark PeakmanDepartment of Immunobiology, Faculty of Life Sciences & Medicine, King's College London, 2nd Floor, Borough Wing, Guy's Hospital, London, UK.ORCID 0000-0003-3328-3513
Iria Gomez-TourinoDepartment of Immunobiology, Faculty of Life Sciences & Medicine, King's College London, 2nd Floor, Borough Wing, Guy's Hospital, London, UK. iria.gomez.tourino@usc.es.ORCID 0000-0001-6594-6110

Funding

Consellería de Cultura, Educación e Ordenación Universitaria, Xunta de Galicia (Ministry of Culture, Education and University Planning, Government of Galicia) ED481A 2022/422EC | EC Seventh Framework Programm | FP7 People: Marie-Curie Actions (FP7-PEOPLE - Specific Programme "People" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)) PIEF-GA-2012-327908Xunta de Galicia ED431C 2023/28
6 · The paper itself

Abstract

Autoimmune diseases result from autoantigen-mediated activation of adaptive immunity; intriguingly, autoantigen-specific T cells are also present in healthy donors. An assessment of dynamic changes of this autoreactive repertoire in both health and disease is thus warranted. Here we investigate the physiological versus pathogenic autoreactive processes in the context of Type 1 diabetes (T1D) and one of its landmark autoantigens, glutamic acid decarboxylase 65 (GAD65). Using single cell gene expression profiling and tandem T cell receptor (TCR) sequencing, we find that GAD65-specific true naïve cells are present in both health and disease, with GAD65-specific effector and memory responses showing similar ratios in healthy donors and patients. Deeper assessment of phenotype and TCR repertoire uncover differential features in GAD65-specific TCRs, including lower clonal sizes of healthy donor-derived clonotypes in patients. We thus propose a model whereby physiological autoimmunity against GAD65 is needed during early life, and that alterations of these physiological autoimmune processes in predisposed individuals trigger overt Type 1 diabetes.

Indexed as

AutoantigensAutoimmunityDiabetes Mellitus, Type 1Glutamate DecarboxylaseReceptors, Antigen, T-CellT-LymphocytesAdolescentAdultChildFemaleGene Expression ProfilingHumansMaleSingle-Cell AnalysisYoung AdultAutoantigensGlutamate Decarboxylaseglutamate decarboxylase 2Receptors, Antigen, T-Cell

Identifiers

PMID39472557
PMCPMC11522472

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.