Evidence map›Paper›PMID 12974753›Full record

ArticleClinical and experimental immunology2003

Dnase1l3 deficiency in lupus-prone MRL and NZB/W F1 mice.

A Wilber, T P O'Connor, M L Lu, A Karimi, M C Schneider

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Clinical and experimental immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Review
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  7. Review
  8. Endosomal Toll-Like Receptors as Therapeutic Targets for Autoimmune Diseases.Advances in experimental medicine and biology · 2024
    Article
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  12. Review
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  19. The cGAS-STING pathway: The role of self-DNA sensing in inflammatory lung disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Review
  20. 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

5 authors at 3 institutions in 1 country.

A WilberDivision of Genetics and Metabolism, Southern Illinois University School of Medicine, Springfield, IL 62794, USA.
T P O'Connor
M L Lu
A Karimi
M C Schneider
Pediatrics and Genetics · USBrigham and Women's Hospital · USSouthern Illinois University School of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of deoxyribonuclease I (Dnase1) function is associated with systemic lupus erythematosus (SLE) in humans and mice; however, no coding mutations in Dnase1 are found in polygenic murine models. Instead, both MRL-lpr strains and NZB/W F1 hybrids are homozygous for T89I missense in the macrophage-DNASE, desoxyribonuclease I-like 3 (Dnase1l3). By in vitro expression studies, this substitution decreases this enzyme's nuclease activity against free DNA by only approximately twofold; however, the mutation has a greater effect on the capacity of media conditioned with Dnase1l3 to confer a barrier to liposomal gene transfection to HeLa cells. The 89I substitution decreases the Dnase1l3 barrier function in vitro by eightfold (P < 0.01). In splenocytes and BM-derived macrophages of SLE mice, while cellular Dnase1l3 levels are induced relative to C57BL/6 (control) mice, levels of FD-nuclease activity are similar. Finally, media conditioned by MRL and NZB/W F1 macrophages, relative to control, contains a weak interferon-gamma (IFN-gamma) inducible Dnase1l3-associated barrier to transfection. This barrier function is hypothesized to reflect the inability of SLE mice to degrade membrane-enveloped DNA-associated antigens, such as apoptotic bodies, which are predicted to stimulate the characteristic autoimmunity of SLE. Our results for these two generally independent models strongly suggest that Dnase1l3 deficiency increases the susceptibility of these mice to polygenic SLE.

Indexed as

Mutation, MissenseAnimalsEndodeoxyribonucleasesFemaleImmunoblottingImmunoglobulin FragmentsLupus Erythematosus, SystemicMacrophagesMaleMiceMice, Mutant StrainsModels, AnimalSequence Analysis, DNATransfectionEndodeoxyribonucleasesImmunoglobulin Fragmentsimmunoglobulins, Fd

Identifiers

PMID12974753
PMCPMC1808827
OpenAlexW2095155160

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.