Evidence map›Paper›PMID 20506216›Full record

ArticleArthritis and rheumatism2010

Constitutive overexpression of BAFF in autoimmune-resistant mice drives only some aspects of systemic lupus erythematosus-like autoimmunity.

William Stohl, Noam Jacob, Shunhua Guo, Laurence Morel

Open access · greenAbstract read
In one paragraph

Article in Arthritis and rheumatism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Article
  3. Loss-of-function variants inAnnals of the rheumatic diseases · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. The function of BAFF on T helper cells in autoimmunity.Cytokine & growth factor reviews · 2014
    Review
  8. Article
  9. Article
  10. An update on belimumab for the treatment of lupus.Biologics : targets & therapy · 2011
    Article
  11. 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

4 authors at 2 institutions in 1 country.

William StohlDivision of Rheumatology, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA. stohl@usc.edu
Noam Jacob
Shunhua Guo
Laurence Morel
University of Southern California · USUniversity of Florida · US

Funding

Characterization of SLE-susceptibility loci on mouse chromosome 1R01AI045050 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Laurence Morel · 2000 to 2026
$11.5M
The vital role of BAFF in the development of SLER01AR050193 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STOHL, WILLIAM · 2006 to 2010
$1.7M
NIAID NIH HHS R01 AI045050NIAID NIH HHS R01-AI-045050NIAMS NIH HHS R01 AR050193NIAMS NIH HHS R01-AR-050193
6 · The paper itself

Abstract

objectiveTo determine whether overexpression of BAFF can promote systemic lupus erythematosus (SLE)-like autoimmunity in mice that are otherwise autoimmune-resistant.

methodsWe used class II major histocompatibility complex (MHC)-deficient C57BL/6 (B6) mice as a model of resistance to SLE and Sles1-bearing B6 mice as a model of resistance to the autoantibody-promoting capacity of the Sle1 region. We generated BAFF-transgenic (Tg) counterparts to these respective mice and evaluated lymphocyte phenotype, serologic autoimmunity, renal immunopathology, and clinical disease in the BAFF-Tg and non-Tg mouse sets.

resultsAlthough constitutive BAFF overexpression did not lead to B cell expansion in class II MHC-deficient B6 mice, it did lead to increased serum IgG autoantibody levels. Nevertheless, renal immunopathology was limited, and clinical disease did not develop. In B6 and B6.Sle1 mice, constitutive BAFF overexpression led to increased numbers of B cells and CD4+ memory cells, as well as increased serum IgG and IgA autoantibody levels. Renal immunopathology was modestly greater in BAFF-Tg mice than in their non-Tg counterparts, but again, clinical disease did not develop. Introduction of the Sles1 region into B6.Sle1.Baff mice abrogated the BAFF-driven increase in CD4+ memory cells and the Sle1-driven, but not the BAFF-driven, increase in serum IgG antichromatin levels. Renal immunopathology was substantially ameliorated.

conclusionAlthough constitutive BAFF overexpression in otherwise autoimmune-resistant mice led to humoral autoimmunity, meaningful renal immunopathology and clinical disease did not develop. This raises the possibility that BAFF overexpression, even when present, may not necessarily drive disease in some SLE patients. This may help explain the heterogeneity of the clinical response to BAFF antagonists in human SLE.

Indexed as

Analysis of VarianceAnimalsAutoantibodiesAutoimmunityB-Cell Activating FactorB-LymphocytesFluorescent Antibody TechniqueKidneyLupus Erythematosus, SystemicMiceMice, Inbred C57BLMice, TransgenicAutoantibodiesB-Cell Activating FactorTnfsf13b protein, mouse

Identifiers

PMID20506216
PMCPMC2921019
OpenAlexW2008172097

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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.