Evidence map›Paper›PMID 37907556›Full record

ArticleNature communications2023

Antigen presentation by B cells enables epitope spreading across an MHC barrier.

Cecilia Fahlquist-Hagert, Thomas R Wittenborn, Ewa Terczyńska-Dyla, Kristian Savstrup Kastberg, Emily Yang, Alysa Nicole Rallistan, Quinton Raymond Markett, Gudrun Winther, Sofie Fonager, Lasse F Voss and 13 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

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  11. Dynamic control of autoreactive B cells from spontaneous germinal centers.Journal of immunology (Baltimore, Md. : 1950) · 2025
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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

23 authors at 6 institutions in 3 countries.

Cecilia Fahlquist-Hagert *Laboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0003-3850-4848
Thomas R Wittenborn *Laboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0002-6361-542X
Ewa Terczyńska-DylaLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.
Kristian Savstrup KastbergLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0002-4467-2736
Emily YangDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA, USA.ORCID 0000-0002-6028-2455
Alysa Nicole RallistanDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA, USA.
Quinton Raymond MarkettDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA, USA.ORCID 0009-0009-4841-1873
Gudrun WintherLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0003-1852-7567
Sofie FonagerLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.
Lasse F VossLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0003-0904-6753
Mathias K PedersenLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0009-0006-7185-2042
Nina van CampenLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0001-5134-9956
Alexey FerapontovLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.
Lisbeth JensenLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.
Jinrong HuangDREAM Laboratory for Applied Genome Technologies, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0001-8085-9939
John D NielandDepartment of Health Science and Technology, Faculty of Medicine, Aalborg University, Gistrup, Denmark.ORCID 0000-0001-7423-0122
Cees E van der PoelProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA, USA.
Johan PalmfeldtResearch Unit for Molecular Medicine, Department of Clinical Medicine, Aarhus University, Aarhus N, Denmark.ORCID 0000-0001-5585-639X
Michael C CarrollProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA, USA.ORCID 0000-0002-3213-4295
Paul J UtzDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA, USA.ORCID 0000-0003-1181-1565
Yonglun LuoDREAM Laboratory for Applied Genome Technologies, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0002-0007-7759
Lin LinDREAM Laboratory for Applied Genome Technologies, Department of Biomedicine, Aarhus University, Aarhus C, Denmark.ORCID 0000-0002-7546-4948
Søren E DegnLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus C, Denmark. sdegn@biomed.au.dk.ORCID 0000-0001-5409-045X
Aarhus University · DKStanford University · USBoston Children's Hospital · USSteno Diabetes Centers · DKAalborg University · DKRadboud University Nijmegen · NL

Funding

Giant MagnetoResistive (GMR) Sensors for Measuring Influenza VaccineR01AI125197 · NIAID · STANFORD UNIVERSITY · PI UTZ, PAUL JOSEPH, WANG, SHAN X. · 2016 to 2021
$5.0M
NIAID NIH HHS R01 AI125197
6 · The paper itself

Abstract

Circumstantial evidence suggests that B cells may instruct T cells to break tolerance. Here, to test this hypothesis, we used a murine model in which a single B cell clone precipitates an autoreactive response resembling systemic lupus erythematosus (SLE). The initiating clone did not need to enter germinal centers to precipitate epitope spreading. Rather, it localized to extrafollicular splenic bridging channels early in the response. Autoantibody produced by the initiating clone was not sufficient to drive the autoreactive response. Subsequent epitope spreading depended on antigen presentation and was compartmentalized by major histocompatibility complex (MHC). B cells carrying two MHC haplotypes could bridge the MHC barrier between B cells that did not share MHC. Thus, B cells directly relay autoreactivity between two separate compartments of MHC-restricted T cells, leading to inclusion of distinct B cell populations in germinal centers. Our findings demonstrate that B cells initiate and propagate the autoimmune response.

Indexed as

Antigen PresentationLupus Erythematosus, SystemicAnimalsB-LymphocytesEpitopesHistocompatibility AntigensHistocompatibility Antigens Class IIMajor Histocompatibility ComplexMiceEpitopesHistocompatibility AntigensHistocompatibility Antigens Class II

Identifiers

PMID37907556
PMCPMC10618542
OpenAlexW4388043123

What OpenQuestion holds

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Registered trials

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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.