Evidence map›Paper›PMID 12642605›Full record

ArticleThe Journal of experimental medicine2003

Type-I interferon receptor deficiency reduces lupus-like disease in NZB mice.

Marie-Laure Santiago-Raber, Roberto Baccala, Katarina M Haraldsson, Divaker Choubey, Timothy A Stewart, Dwight H Kono, Argyrios N Theofilopoulos

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 222 papers.

0numbers the graph read from it
0cells of the map it votes in
222citing papers in PubMed
22.6field-weighted citation impact, top 1% 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

222 citing papers in PubMed, 504 citations in OpenAlex.

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  19. The solute carrier SLC15A4 is required for optimal trafficking of nucleic acid-sensing TLRs and ligands to endolysosomes.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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162 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Marie-Laure Santiago-RaberDepartment of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Roberto Baccala
Katarina M Haraldsson
Divaker Choubey
Timothy A Stewart
Dwight H Kono
Argyrios N Theofilopoulos
Scripps Research Institute · USGene Therapy Laboratory · FRLoyola University Medical Center · US

Funding

T Cell Homeostasis in Systemic AutoimmunityR01AR031203 · NIAMS · SCRIPPS RESEARCH INSTITUTE, THE · PI THEOFILOPOULOS, ARGYRIOS N · 1986 to 2012
$4.9M
Genetic Basis of Systemic AutoimmunityR37AR039555 · NIAMS · SCRIPPS RESEARCH INSTITUTE, THE · PI THEOFILOPOULOS, ARGYRIOS N · 2003 to 2012
$4.2M
T CELL ANTIGEN RECEPTOR GENES IN AUTOIMMUNITYR01AR039555 · NIAMS · SCRIPPS RESEARCH INSTITUTE · PI THEOFILOPOULOS, ARGYRIOS N · 1988 to 2002
$1.4M
NIAMS NIH HHS AR31203NIAMS NIH HHS AR39555NIAMS NIH HHS R01 AR031203NIAMS NIH HHS R01 AR039555NIAMS NIH HHS R37 AR039555
6 · The paper itself

Abstract

Indirect evidence suggests that type-I interferons (IFN-alpha/beta) play a significant role in the pathogenesis of lupus. To directly examine the contribution of these pleiotropic molecules, we created congenic NZB mice lacking the alpha-chain of IFN-alpha/betaR, the common receptor for the multiple IFN-alpha/beta species. Compared with littermate controls, homozygous IFN-alpha/betaR-deleted NZB mice had significantly reduced anti-erythrocyte autoantibodies, erythroblastosis, hemolytic anemia, anti-DNA autoantibodies, kidney disease, and mortality. These reductions were intermediate in the heterozygous-deleted mice. The disease-ameliorating effects were accompanied by reductions in splenomegaly and in several immune cell subsets, including B-1 cells, the major producers of anti-erythrocyte autoantibodies. Decreases of B and T cell proliferation in vitro and in vivo, and of dendritic cell maturation and T cell stimulatory activity in vitro were also detected. Absence of signaling through the IFN-alpha/betaR, however, did not affect increased basal levels of the IFN-responsive p202 phosphoprotein, encoded by a polymorphic variant of the Ifi202 gene associated with the Nba2 predisposing locus in NZB mice. The data indicate that type-I IFNs are important mediators in the pathogenesis of murine lupus, and that reducing their activity in the human counterpart may be beneficial.

Indexed as

AnimalsAntibody-Producing CellsDendritic CellsDNAFemaleHumansImmunoglobulinsInterferon-alphaInterferon-betaKidneyLupus Erythematosus, SystemicLymphocyte SubsetsMembrane ProteinsMiceMice, Inbred BALB CMice, Inbred NZBDNAImmunoglobulinsInterferon-alphaInterferon-betaMembrane ProteinsReceptor, Interferon alpha-betaReceptors, Interferon

Identifiers

PMID12642605
PMCPMC2193854
OpenAlexW2016899230

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.