Evidence map›Paper›PMID 31150624›Full record

ArticleCell2019

A Public BCR Present in a Unique Dual-Receptor-Expressing Lymphocyte from Type 1 Diabetes Patients Encodes a Potent T Cell Autoantigen.

Rizwan Ahmed, Zahra Omidian, Adebola Giwa, Benjamin Cornwell, Neha Majety, David R Bell, Sangyun Lee, Hao Zhang, Aaron Michels, Stephen Desiderio and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
7.0field-weighted citation impact, top 2% of its field
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

72 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
  2. Article
  3. A distinct TCRiScience · 2026
    Article
  4. Donor-derived CD8bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Observational
  11. Article
  12. Article
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  15. Review
  16. Article
  17. Article
  18. Article
  19. B-Cell Receptor Repertoire: Recent Advances in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2024
    Review
  20. Article

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 7 institutions in 1 country.

Rizwan AhmedDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Zahra OmidianDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Adebola GiwaDepartment of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Benjamin CornwellDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Neha MajetyDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
David R BellComputational Biology Center, IBM Thomas J. Watson Research Center, Yorktown Heights, NY 10598, USA.
Sangyun LeeComputational Biology Center, IBM Thomas J. Watson Research Center, Yorktown Heights, NY 10598, USA.
Hao ZhangDepartment of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Aaron MichelsBarbara Davis Center for Diabetes, University of Colorado, Aurora, CO 80045, USA.
Stephen DesiderioDepartment of Molecular Biology and Genetics and Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Scheherazade Sadegh-NasseriDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Hamid RabbDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Simon GritschDepartment of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Mario L SuvaDepartment of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.
Patrick CahanDepartment of Molecular Biology and Genetics and Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Ruhong ZhouComputational Biology Center, IBM Thomas J. Watson Research Center, Yorktown Heights, NY 10598, USA; Department of Chemistry, Columbia University, New York, NY 10027, USA. Electronic address: rz24@columbia.edu.
Chunfa JieDepartment of Biochemistry and Nutrition, Des Moines University, Des Moines, IA 50312, USA.
Thomas DonnerDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Abdel Rahim A HamadDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: ahamad@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · USIBM Research - Thomas J. Watson Research Center · USBroad Institute · USCenter for Cancer Research · USDes Moines University · USUniversity of Colorado Denver · US

Funding

Institutional Training for PediatriciansT32HD044355 · NICHD · JOHNS HOPKINS UNIVERSITY · PI BRADY, TAMMY MCLOUGHLIN · 2003 to 2023
$4.1M
Mechanisms of Fas Ligand Control of Insulitis in Autoimmune DiabetesR01AI099027 · NIAID · JOHNS HOPKINS UNIVERSITY · PI HAMAD, ABDEL RAHIM · 2013 to 2017
$2.0M
Understanding the Impacts of HLA-DO in vivoR01AI120634 · NIAID · JOHNS HOPKINS UNIVERSITY · PI SADEGH-NASSERI, SCHEHERAZADE · 2016 to 2019
$1.6M
NIAID NIH HHS R01 AI099027NIAID NIH HHS R01 AI120634NICHD NIH HHS T32 HD044355
6 · The paper itself

Abstract

T and B cells are the two known lineages of adaptive immune cells. Here, we describe a previously unknown lymphocyte that is a dual expresser (DE) of TCR and BCR and key lineage markers of both B and T cells. In type 1 diabetes (T1D), DEs are predominated by one clonotype that encodes a potent CD4 T cell autoantigen in its antigen binding site. Molecular dynamics simulations revealed that this peptide has an optimal binding register for diabetogenic HLA-DQ8. In concordance, a synthetic version of the peptide forms stable DQ8 complexes and potently stimulates autoreactive CD4 T cells from T1D patients, but not healthy controls. Moreover, mAbs bearing this clonotype are autoreactive against CD4 T cells and inhibit insulin tetramer binding to CD4 T cells. Thus, compartmentalization of adaptive immune cells into T and B cells is not absolute, and violators of this paradigm are likely key drivers of autoimmune diseases.

Indexed as

AdolescentAdultAutoantigensB-LymphocytesCD4-Positive T-LymphocytesChildChild, PreschoolDiabetes Mellitus, Type 1EpitopesFemaleHEK293 CellsHLA-DQ AntigensHumansLymphocyte ActivationLymphocytesMaleAutoantigensEpitopesHLA-DQ8 antigenHLA-DQ AntigensPeptidesautoantigenDEsdual expressersinsulin mimotopeislet autoantigentype 1 diabetesx-clonotypex-idiotype

Identifiers

PMID31150624
PMCPMC7962621
OpenAlexW2947468286

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.