Evidence map›Paper›PMID 15314659›Full record

ArticlePLoS biology2004

Spontaneous autoimmunity in 129 and C57BL/6 mice-implications for autoimmunity described in gene-targeted mice.

Anne E Bygrave, Kirsten L Rose, Josefina Cortes-Hernandez, Joanna Warren, Robert J Rigby, H Terence Cook, Mark J Walport, Timothy J Vyse, Marina Botto

Abstract read
In one paragraph

Article in PLoS biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

87 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  15. Expression of a constitutively active humanLife science alliance · 2019
    Article
  16. Review
  17. Review
  18. DNA as a self-antigen: nature and regulation.Current opinion in immunology · 2018
    Review
  19. A Restricted Role for FcγR in the Regulation of Adaptive Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  20. Review

27 more citing papers are in PubMed but not listed here.

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

9 authors.

Anne E BygraveRheumatology Section, Eric Bywaters Centre, Imperial College, London, United Kingdom.
Kirsten L Rose
Josefina Cortes-Hernandez
Joanna Warren
Robert J Rigby
H Terence Cook
Mark J Walport
Timothy J Vyse
Marina Botto

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder in which complex genetic factors play an important role. Several strains of gene-targeted mice have been reported to develop SLE, implicating the null genes in the causation of disease. However, hybrid strains between 129 and C57BL/6 mice, widely used in the generation of gene-targeted mice, develop spontaneous autoimmunity. Furthermore, the genetic background markedly influences the autoimmune phenotype of SLE in gene-targeted mice. This suggests an important role in the expression of autoimmunity of as-yet-uncharacterised background genes originating from these parental mouse strains. Using genome-wide linkage analysis, we identified several susceptibility loci, derived from 129 and C57BL/6 mice, mapped in the lupus-prone hybrid (129 x C57BL/6) model. By creating a C57BL/6 congenic strain carrying a 129-derived Chromosome 1 segment, we found that this 129 interval was sufficient to mediate the loss of tolerance to nuclear antigens, which had previously been attributed to a disrupted gene. These results demonstrate important epistatic modifiers of autoimmunity in 129 and C57BL/6 mouse strains, widely used in gene targeting. These background gene influences may account for some, or even all, of the autoimmune traits described in some gene-targeted models of SLE.

Indexed as

Models, GeneticAnimalsAutoimmunityCell NucleusChromosome MappingCohort StudiesDisease Models, AnimalEpistasis, GeneticFemaleGene TargetingGenetic LinkageGenetic Predisposition to DiseaseGenomeGenotypeLupus Erythematosus, SystemicMice

Identifiers

PMID15314659
PMCPMC509305

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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.