Evidence map›Paper›PMID 20018631›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Development of murine lupus involves the combined genetic contribution of the SLAM and FcgammaR intervals within the Nba2 autoimmune susceptibility locus.

Trine N Jørgensen, Jennifer Alfaro, Hilda L Enriquez, Chao Jiang, William M Loo, Stephanie Atencio, Melanie R Gubbels Bupp, Christina M Mailloux, Troy Metzger, Shannon Flannery and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.1field-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

40 citing papers in PubMed, 68 citations in OpenAlex.

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  12. Absent in Melanoma 2 proteins in SLE.Clinical immunology (Orlando, Fla.) · 2017
    Review
  13. Review
  14. Article
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  19. B cell-intrinsic CD84 and Ly108 maintain germinal center B cell tolerance.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 3 countries.

Trine N JørgensenDivision of Allergy and Clinical Immunology, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
Jennifer Alfaro
Hilda L Enriquez
Chao Jiang
William M Loo
Stephanie Atencio
Melanie R Gubbels Bupp
Christina M Mailloux
Troy Metzger
Shannon Flannery
Stephen J Rozzo
Brian L Kotzin
Mario Rosemblatt
María Rosa Bono
Loren D Erickson
University of Colorado Health · USUniversity of Virginia · USUniversidad de Santiago de Chile · CL

Funding

Pathways of plasma cell differentiation in autoimmunityR01AI093722 · NIAID · UNIVERSITY OF VIRGINIA · PI ERICKSON, LOREN D · 2012 to 2016
$2.0M
GENETICS OF AUTOIMMUNITYR01AR037070 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI KOTZIN, BRIAN L · 1986 to 2003
$1.2M
Role of TLRs in plasma cell differentiation and survivalR03AR052902 · NIAMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI ERICKSON, LOREN D · 2005 to 2007
$222k
NIAID NIH HHS R01 AI093722NIAMS NIH HHS 5R01AR37070-19NIAMS NIH HHS AR052902NIAMS NIH HHS R01 AR037070NIAMS NIH HHS R03 AR052902
6 · The paper itself

Abstract

Autoantibodies are of central importance in the pathogenesis of Ab-mediated autoimmune disorders. The murine lupus susceptibility locus Nba2 on chromosome 1 and the syntenic human locus are associated with a loss of immune tolerance that leads to antinuclear Ab production. To identify gene intervals within Nba2 that control the development of autoantibody-producing B cells and to determine the cellular components through which Nba2 genes accomplish this, we generated congenic mice expressing various Nba2 intervals where genes for the FcgammaR, SLAM, and IFN-inducible families are encoded. Analysis of congenic strains demonstrated that the FcgammaR and SLAM intervals independently controlled the severity of autoantibody production and renal disease, yet are both required for lupus susceptibility. Deregulated homeostasis of terminally differentiated B cells was found to be controlled by the FcgammaR interval where FcgammaRIIb-mediated apoptosis of germinal center B cells and plasma cells was impaired. Increased numbers of activated plasmacytoid dendritic cells that were distinctly CD19+ and promoted plasma cell differentiation via the proinflammatory cytokines IL-10 and IFNalpha were linked to the SLAM interval. These findings suggest that SLAM and FcgammaR intervals act cooperatively to influence the clinical course of disease through supporting the differentiation and survival of autoantibody-producing cells.

Indexed as

AnimalsAntigens, CDApoptosisAutoantibodiesB-LymphocytesCell DifferentiationCytokinesDisease ProgressionGenetic Predisposition to DiseaseKidney DiseasesLupus Erythematosus, SystemicMiceMice, CongenicPlasma CellsReceptors, Cell SurfaceReceptors, IgGAntigens, CDAutoantibodiesCytokinesReceptors, Cell SurfaceReceptors, IgGSignaling Lymphocytic Activation Molecule Family Member 1

Identifiers

PMID20018631
PMCPMC2841050
OpenAlexW2107349643

What OpenQuestion holds

Textmetadata
LicenceTDM
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.