Evidence map›Paper›PMID 29996101›Full record

ArticleCell reports2018

B-Cell-Intrinsic Type 1 Interferon Signaling Is Crucial for Loss of Tolerance and the Development of Autoreactive B Cells.

Phillip P Domeier, Sathi Babu Chodisetti, Stephanie L Schell, Yuka Imamura Kawasawa, Melinda J Fasnacht, Chetna Soni, Ziaur S M Rahman

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

68 citing papers in PubMed, 104 citations in OpenAlex.

  1. Review
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  12. NETosis: A key player in autoimmunity, COVID-19, and long COVID.Journal of translational autoimmunity · 2025
    Review
  13. Article
  14. Review
  15. Article
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  17. Immune Checkpoints in B Cells: Unlocking New Potentials in Cancer Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  18. Article
  19. Review
  20. Article

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

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

7 authors at 1 institution in 1 country.

Phillip P DomeierDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA.
Sathi Babu ChodisettiDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA.
Stephanie L SchellDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA.
Yuka Imamura KawasawaDepartments of Pharmacology and Biochemistry and Molecular Biology, Institute for Personalized Medicine, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA.
Melinda J FasnachtDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA.
Chetna SoniDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA.
Ziaur S M RahmanDepartment of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA. Electronic address: zrahman@pennstatehealth.psu.edu.
Pennsylvania State University · US

Funding

"Perturbation of peripheral B cell tolerance by the lupus susceptibility loci"R01AI091670 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI RAHMAN, ZIAUR · 2011 to 2015
$1.9M
B-cell intrinsic Type 1 and Type 2 interferon signaling in regulating spontaneous germinal centers and autoimmunityF31AI122608 · NIAID · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI DOMEIER, PHILLIP P · 2016 to 2017
$75k
NIAID NIH HHS F31 AI122608NIAID NIH HHS R01 AI091670
6 · The paper itself

Abstract

Type 1 interferon (T1IFN) signaling promotes inflammation and lupus pathology, but its role in autoreactive B cell development in the antibody-forming cell (AFC) and germinal center (GC) pathways is unclear. Using a lupus model that allows for focused study of the AFC and GC responses, we show that T1IFN signaling is crucial for autoreactive B cell development in the AFC and GC pathways. Through bone marrow chimeras, DNA-reactive B cell transfer, and GC-specific Cre mice, we confirm that IFNαR signaling in B cells promotes autoreactive B cell development into both pathways. Transcriptomic analysis reveals gene expression alterations in multiple signaling pathways in non-GC and GC B cells in the absence of IFNαR. Finally, we find that T1IFN signaling promotes autoreactive B cell development in the AFC and GC pathways by regulating BCR signaling. These data suggest value for anti-IFNαR therapy in individuals with elevated T1IFN activity before clinical disease onset.

Indexed as

Immune ToleranceSignal TransductionAnimalsAntibodies, AntinuclearAntibody AffinityAntibody FormationAntigensAutoantibodiesB-LymphocytesDNAFemaleGerminal CenterImmunizationInterferon Type IMice, Inbred C57BLReceptor, Interferon alpha-betaAntibodies, AntinuclearAntigensAutoantibodiesDNAIfnar1 protein, mouseInterferon Type IReceptor, Interferon alpha-betaantibody-forming cellsautoimmunityB cellsB cell tolerancespontaneous germinal centerssystemic lupus erythematosustype 1 interferon signaling

Identifiers

PMID29996101
PMCPMC6089613
OpenAlexW2825313082

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.