Evidence map›Paper›PMID 34795279›Full record

ArticleNature communications2021

Follicular T cells are clonally and transcriptionally distinct in B cell-driven mouse autoimmune disease.

Elliot H Akama-Garren, Theo van den Broek, Lea Simoni, Carlos Castrillon, Cees E van der Poel, Michael C Carroll

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  3. Article
  4. Article
  5. Review
  6. Article
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  9. Article
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  11. T cell help shapes B cell tolerance.Science immunology · 2024
    Article
  12. Article
  13. Article
  14. Renegade T cell clones and autoimmune disease.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Article
  16. Review
  17. T cell help in the autoreactive germinal center.Scandinavian journal of immunology · 2022
    Review
  18. Article
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

6 authors at 1 institution in 1 country.

Elliot H Akama-GarrenProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.ORCID http://orcid.org/0000-0002-1690-2055
Theo van den BroekProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.ORCID http://orcid.org/0000-0002-2781-5731
Lea SimoniProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Carlos CastrillonProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Cees E van der PoelProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Michael C CarrollProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, 02115, USA. michael.carroll@childrens.harvard.edu.ORCID http://orcid.org/0000-0002-3213-4295
Boston Children's Hospital · US

Funding

Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
TRAINING IN TRANSPLANTATION BIOLOGYT32AI007529 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI MADSEN, JOREN C · 1998 to 2024
$6.4M
Evolution of autoreactive GC and epitope spreading in lupusR01AR074105 · NIAMS · BOSTON CHILDREN'S HOSPITAL · PI Michael Craig Carroll · 2018 to 2026
$4.2M
Follicular helper T cells as drivers of epitope spreadingF30AI160909 · NIAID · HARVARD MEDICAL SCHOOL · PI AKAMA-GARREN, ELLIOT HIDEKI · 2021 to 2023
$125k
NIAID NIH HHS F30 AI160909NIAID NIH HHS T32 AI007529NIAMS NIH HHS R01 AR074105NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

Pathogenic autoantibodies contribute to tissue damage and clinical decline in autoimmune disease. Follicular T cells are central regulators of germinal centers, although their contribution to autoantibody-mediated disease remains unclear. Here we perform single cell RNA and T cell receptor (TCR) sequencing of follicular T cells in a mouse model of autoantibody-mediated disease, allowing for analyses of paired transcriptomes and unbiased TCRαβ repertoires at single cell resolution. A minority of clonotypes are preferentially shared amongst autoimmune follicular T cells and clonotypic expansion is associated with differential gene signatures in autoimmune disease. Antigen prediction using algorithmic and machine learning approaches indicates convergence towards shared specificities between non-autoimmune and autoimmune follicular T cells. However, differential autoimmune transcriptional signatures are preserved even amongst follicular T cells with shared predicted specificities. These results demonstrate that follicular T cells are phenotypically distinct in B cell-driven autoimmune disease, providing potential therapeutic targets to modulate autoantibody development.

Indexed as

AnimalsAutoimmune DiseasesB-LymphocytesCD4-Positive T-LymphocytesCells, CulturedClone CellsGene Expression ProfilingGerminal CenterMiceMice, Inbred C57BLMicroscopy, ConfocalReceptors, Antigen, T-CellReverse Transcriptase Polymerase Chain ReactionRNA-SeqSingle-Cell AnalysisT-Lymphocytes, Helper-InducerReceptors, Antigen, T-Cell

Identifiers

PMID34795279
PMCPMC8602266
OpenAlexW3213415363

What OpenQuestion holds

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LicenceCC BY
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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.