Evidence map›Paper›PMID 26694971›Full record

ArticleThe Journal of experimental medicine2016

Receptor editing and genetic variability in human autoreactive B cells.

Julie Lang, Takayuki Ota, Margot Kelly, Pamela Strauch, Brian M Freed, Raul M Torres, David Nemazee, Roberta Pelanda

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2016. 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
–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

27 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. SARS-CoV-2 infection relaxes peripheral B cell tolerance.The Journal of experimental medicine · 2022
    Article
  5. Review
  6. Review
  7. Article
  8. Central human B cell tolerance manifests with a distinctive cell phenotype and is enforced via CXCR4 signaling in hu-mice.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Anti-HIV-1 B cell responses are dependent on B cell precursor frequency and antigen-binding affinity.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  20. 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

8 authors.

Julie LangDepartment of Immunology and Microbiology, University of Colorado Denver School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
Takayuki OtaDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037.
Margot KellyDepartment of Immunology and Microbiology, University of Colorado Denver School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
Pamela StrauchDepartment of Immunology and Microbiology, University of Colorado Denver School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
Brian M FreedDepartment of Immunology and Microbiology, University of Colorado Denver School of Medicine, Aurora, CO 80045 Division of Allergy and Clinical Immunology, University of Colorado Denver School of Medicine, Aurora, CO 80045.
Raul M TorresDepartment of Immunology and Microbiology, University of Colorado Denver School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
David NemazeeDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037.
Roberta PelandaDepartment of Immunology and Microbiology, University of Colorado Denver School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206 Roberta.Pelanda@ucdenver.edu.

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
THE REGULATION OF V ALPHA 7 EXPRESSING T CELLSP01AI022295 · NIAID · NATIONAL JEWISH HEALTH · PI REFAELI, YOSEF · 1985 to 2011
$11.7M
Chemokine response in B cell development and functionR01AI052157 · NIAID · UNIVERSITY OF COLORADO DENVER · PI TORRES, RAUL MARTIN · 2002 to 2017
$5.4M
Tolerance in Polyclonal and Oligoclonal Immune SystemsR01AI052310 · NIAID · UNIVERSITY OF COLORADO DENVER · PI PELANDA, ROBERTA · 2003 to 2017
$5.0M
Immune Tolerance in Non-Clonal Immune SystemsR01AI059714 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 2004 to 2013
$3.9M
Immune Tolerance in Non-Clonal Immune SystemsR37AI059714 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 2014 to 2020
$3.5M
Studies of human B cell tolerance, from a humanized mouse model to human beingsR01AI124474 · NIAID · UNIVERSITY OF COLORADO DENVER · PI PELANDA, ROBERTA · 2016 to 2020
$2.3M
Analysis of Human B Cell Tolerance in Humanized MiceR21AI073629 · NIAID · NATIONAL JEWISH HEALTH · PI PELANDA, ROBERTA · 2008 to 2009
$451k
NCI NIH HHS P30 CA046934NCI NIH HHS P30CA046934NIAID NIH HHS P01 AI022295NIAID NIH HHS R01 AI052157NIAID NIH HHS R01 AI052310NIAID NIH HHS R01 AI059714NIAID NIH HHS R01 AI124474NIAID NIH HHS R01-AI59714NIAID NIH HHS R21 AI073629NIAID NIH HHS R21-AI073629NIAID NIH HHS R37 AI059714
6 · The paper itself

Abstract

The mechanisms by which B cells undergo tolerance, such as receptor editing, clonal deletion, and anergy, have been established in mice. However, corroborating these mechanisms in humans remains challenging. To study how autoreactive human B cells undergo tolerance, we developed a novel humanized mouse model. Mice expressing an anti-human Igκ membrane protein to serve as a ubiquitous neo self-antigen (Ag) were transplanted with a human immune system. By following the fate of self-reactive human κ(+) B cells relative to nonautoreactive λ(+) cells, we show that tolerance of human B cells occurs at the first site of self-Ag encounter, the bone marrow, via a combination of receptor editing and clonal deletion. Moreover, the amount of available self-Ag and the genetics of the cord blood donor dictate the levels of central tolerance and autoreactive B cells in the periphery. Thus, this model can be useful for studying specific mechanisms of human B cell tolerance and to reveal differences in the extent of this process among human populations.

Indexed as

Genetic VariationAnimalsAntigens, CD19AutoantigensAutoimmunityB-LymphocytesB-Lymphocyte SubsetsHumansImmune ToleranceImmunoglobulin kappa-ChainsImmunoglobulin lambda-ChainsImmunophenotypingMiceMice, TransgenicReceptors, Antigen, B-CellAntigens, CD19AutoantigensImmunoglobulin kappa-ChainsImmunoglobulin lambda-ChainsReceptors, Antigen, B-Cell

Identifiers

PMID26694971
PMCPMC4710202

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.