Evidence map›Paper›PMID 23334904›Full record

ArticleArthritis and rheumatism2013

Development of systemic lupus erythematosus in NZM 2328 mice in the absence of any single BAFF receptor.

Chaim O Jacob, Ning Yu, Shunhua Guo, Noam Jacob, William J Quinn, Vishal Sindhava, Michael P Cancro, Beatrice Goilav, Chaim Putterman, Thi-Sau Migone and 1 more

Open access · greenAbstract read
In one paragraph

Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.5field-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

19 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Inhibition of B cell activation followingJournal of translational autoimmunity · 2021
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. An update on lupus animal models.Current opinion in rheumatology · 2017
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Expression of BAFF and BR3 in patients with systemic lupus erythematosus.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. The BAFF/APRIL system in SLE pathogenesis.Nature reviews. Rheumatology · 2014
    Review
  19. Review
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

11 authors at 5 institutions in 1 country.

Chaim O JacobUniversity of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA. jacob@usc.edu
Ning Yu
Shunhua Guo
Noam Jacob
William J Quinn
Vishal Sindhava
Michael P Cancro
Beatrice Goilav
Chaim Putterman
Thi-Sau Migone
William Stohl
University of Southern California · USUniversity of Pennsylvania · USAlbert Einstein College of Medicine · USChildren's Hospital at Montefiore · USHuman Genome Sciences (United States) · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
Immune System Development and RegulationT32AI055428 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI ALLMAN, DAVID M, OLIVER, PAULA MARIA · 2003 to 2025
$4.2M
The Renal Pathogenicity of anti-DNA AntibodiesR01AR048692 · NIAMS · YESHIVA UNIVERSITY · PI PUTTERMAN, CHAIM · 2002 to 2013
$4.0M
Transitional B cell selection during peripheral B lymphopenia and reconstitutionR01AI073939 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI CANCRO, MICHAEL PAUL · 2007 to 2011
$2.1M
Cytokine mechanisms in systemic lupus erythematosusR01AI057473 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JACOB, CHAIM O. · 2004 to 2008
$2.0M
The vital role of BAFF in the development of SLER01AR050193 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STOHL, WILLIAM · 2006 to 2010
$1.7M
TNF-like weak inducer of apoptosis (TWEAK) signaling in lupus nephritisR01DK090319 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI PUTTERMAN, CHAIM · 2011 to 2014
$1.5M
NCI NIH HHS P30 CA016520NIAID NIH HHS R01 AI057473NIAID NIH HHS R01-AI-057473NIAID NIH HHS R01 AI073939NIAID NIH HHS R01-AI-073939NIAID NIH HHS T32 AI055428NIAID NIH HHS T32-AI-055428NIAMS NIH HHS R01 AR048692NIAMS NIH HHS R01-AR-048692NIAMS NIH HHS R01 AR050193NIAMS NIH HHS R01-AR-050193NIDDK NIH HHS R01 DK090319NIDDK NIH HHS R01-DK-090319
6 · The paper itself

Abstract

objectiveTo determine the necessity for any individual BAFF receptor in the development of systemic lupus erythematosus (SLE).

methodsBcma-, Taci-, and Br3-null mutations were introgressed into NZM 2328 mice. NZM.Bcma-/-, NZM.Taci-/-, and NZM.Br3-/- mice were evaluated for lymphocyte phenotype and BAFF receptor expression by flow cytometry; for B cell responsiveness to BAFF by in vitro culture; for serum levels of BAFF and total IgG and IgG anti-double-stranded DNA (anti-dsDNA) by enzyme-linked immunosorbent assay; for renal immunopathology by immunofluorescence and histopathology; and for clinical disease.

resultsBCMA, TACI, and B lymphocyte stimulator receptor 3 (BR3) were not surface-expressed in NZM.Bcma-/-, NZM.Taci-/-, and NZM.Br3-/- mice, respectively. Transitional and follicular B cells from NZM.Br3-/- mice were much less responsive to BAFF than were the corresponding cells from wild-type, NZM.Bcma-/-, or NZM.Taci-/- mice. In comparison with wild-type mice, NZM.Bcma-/- and NZM.Taci-/- mice harbored an increased number of spleen B cells, T cells, and plasma cells, whereas serum levels of total IgG and IgG anti-dsDNA were similar to those in wild-type mice. Despite their paucity of B cells, NZM.Br3-/- mice had an increased number of T cells, and the numbers of plasma cells and levels of IgG anti-dsDNA were similar to those in wild-type mice. Serum levels of BAFF were increased in NZM.Taci-/- and NZM.Br3-/- mice but were decreased in NZM.Bcma-/- mice. Despite their phenotypic differences, NZM.Bcma-/-, NZM.Taci-/-, and NZM.Br3-/- mice had renal immunopathology and clinical disease that were at least as severe as that in wild-type mice.

conclusionAny single BAFF receptor, including BR3, is dispensable for the development of SLE in NZM mice. Development of disease in NZM.Br3-/- mice demonstrates that BAFF-BCMA and/or BAFF-TACI interactions contribute to SLE, and that a profound, life-long reduction in the numbers of B cells does not guarantee protection against SLE.

Indexed as

B-Lymphocyte SubsetsAnimalsAntibodies, AntinuclearB-Cell Activating FactorB-Cell Activation Factor ReceptorB-Cell Maturation AntigenDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryImmunoglobulin GImmunoglobulin MKidneyLupus Erythematosus, SystemicMiceMice, CongenicAntibodies, AntinuclearB-Cell Activating FactorB-Cell Activation Factor ReceptorB-Cell Maturation AntigenImmunoglobulin GImmunoglobulin MTnfrsf13b protein, mouseTnfrsf13c protein, mouseTnfrsf17 protein, mouseTnfsf13b protein, mouseTransmembrane Activator and CAML Interactor Protein

Identifiers

PMID23334904
PMCPMC3618582
OpenAlexW1600749829

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.