Evidence map›Paper›PMID 14615579›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

IL-18 cDNA vaccination protects mice from spontaneous lupus-like autoimmune disease.

Paola Bossù, Detlef Neumann, Elda Del Giudice, Antonio Ciaramella, Isabelle Gloaguen, Giamila Fantuzzi, Charles A Dinarello, Emma Di Carlo, Piero Musiani, Pier Luigi Meroni and 3 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The Roles of Interleukin-18 in Inflammation and Autoimmune Disease.Clinical reviews in allergy & immunology · 2026
    Review
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  17. IL-18 Drives ILC3 Proliferation and Promotes IL-22 Production via NF-κB.Journal of immunology (Baltimore, Md. : 1950) · 2017
    Article
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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

13 authors at 3 institutions in 1 country.

Paola BossùLaboratory of Clinical and Behavioral Neurology, Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia, 00179 Rome, Italy.
Detlef Neumann
Elda Del Giudice
Antonio Ciaramella
Isabelle Gloaguen
Giamila Fantuzzi
Charles A Dinarello
Emma Di Carlo
Piero Musiani
Pier Luigi Meroni
Gianfranco Caselli
Paolo Ruggiero
Diana Boraschi
Newron Pharmaceuticals (Italy) · ITConsorzio CREO (Italy) · ITIRCCS Istituto Auxologico Italiano · IT

Funding

Yeast-based HTS Assay Technologies for ProteasesR01AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1985 to 2025
$8.5M
Pathogenesis of Fever in ManR56AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 2016 to 2016
$311k
PATHOGENESIS OF FEVER IN HUMANSR37AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1988 to 1998
–
NIAID NIH HHS AI-15614NIAID NIH HHS R01 AI015614NIAID NIH HHS R56 AI015614
6 · The paper itself

Abstract

The lupus-like autoimmune syndrome of MRL/Mp-Tnfrsf6lpr (lpr) mice is characterized by progressive lymphadenopathy and autoantibody production, leading to early death from renal failure. Activation of T helper lymphocytes is one of the events in the pathogenesis of the disease in these mice and likely in human systemic lupus erythematosus. Among T helper lymphocyte-dependent cytokines, IFN-gamma plays a pivotal role in the abnormal cell activation and the fatal development of the lpr disease. IL-18, an inducer of IFN-gamma in T lymphocytes and natural killer cells, may contribute to the disease because cells from lpr mice are hypersensitive to IL-18 and express high levels of IL-18. To assess the contribution of IL-18 to the pathogenesis in the animal model, in vivo inhibition of IL-18 was attempted. Young lpr mice were vaccinated against autologous IL-18 by repeated administration of a cDNA coding for the murine IL-18 precursor. Vaccinated mice produced autoantibodies to murine IL-18 and exhibited a significant reduction in spontaneous lymphoproliferation and IFN-gamma production as well as less glomerulonephritis and renal damage. Moreover, mortality was significantly delayed in anti-IL-18-vaccinated mice. These studies support the concept that IL-18 plays a major role in the pathogenesis of the autoimmune syndrome of lpr mice and that a reduction in IL-18 activity could be a therapeutic strategy in autoimmune diseases.

Indexed as

AnimalsAutoantibodiesHumansInterferon-gammaInterleukin-18Lupus Erythematosus, SystemicLupus NephritisLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred MRL lprT-LymphocytesVaccines, DNAAutoantibodiesInterferon-gammaInterleukin-18Vaccines, DNA

Identifiers

PMID14615579
PMCPMC283566
OpenAlexW2155661533

What OpenQuestion holds

Textmetadata
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.