Evidence map›Paper›PMID 17728789›Full record

ArticleGenes and immunity2007

Sle3 and Sle5 can independently couple with Sle1 to mediate severe lupus nephritis.

K Liu, Q Z Li, Y Yu, C Liang, S Subramanian, Z Zeng, H W Wang, C Xie, X J Zhou, C Mohan and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. The BAFF/APRIL system in SLE pathogenesis.Nature reviews. Rheumatology · 2014
    Review
  6. B cell-specific loss of Lyn kinase leads to autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Genetics of SLE: evidence from mouse models.Nature reviews. Rheumatology · 2010
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

11 authors at 3 institutions in 1 country.

K LiuDepartment of Immunology, The University of Texas Southwestern Medical Center, Dallas, TX 75390-9093, USA. kui.liu@utsouthwestern.edu
Q Z Li
Y Yu
C Liang
S Subramanian
Z Zeng
H W Wang
C Xie
X J Zhou
C Mohan
E K Wakeland
The University of Texas Southwestern Medical Center · USSouthwestern Medical Center · USUniversity of Florida · US

Funding

Sle triggered disease pathwaysP01AI039824 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI WAKELAND, EDWARD K. · 1996 to 2011
$13.0M
Delineation of genetic pathways to lupus pathogenesisF32AR048058 · NIAMS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI LIU, KUI · 2001 to 2003
$135k
NIAID NIH HHS P01 AI 39824NIAMS NIH HHS 5 F32 AR48058
6 · The paper itself

Abstract

Genetic analyses of the lupus-prone NZM2410 mouse have identified multiple susceptibility loci on chromosome 7, termed Sle3 and Sle5. Both of these loci were contained within a large congenic interval, originally termed as Sle3 that strongly impacts a variety of myeloid and T-cell phenotypes and mediates fatal lupus nephritis when combined with Sle1. We have now produced two subcongenic strains, B6.Sle3 and B6.Sle5, carrying the Sle3 and Sle5 intervals separately and characterized their phenotypes as monocongenic strains and individually in combination with Sle1. Neither B6.Sle3 nor B6.Sle5 monocongenic strain develop severe autoimmunity; however, both of these intervals cause the development of severe glomerulonephritis when combined with Sle1. Thus, B6.Sle1Sle3 and B6.Sle1Sle5 exhibit splenomegaly, expansion of activated B and CD4+ T-cell populations and high levels of IgG and IgM autoantibodies targeting multiple nuclear antigens, intact glomeruli and various other autoantigens. In addition, B6.Sle1Sle3 mice also produced higher levels of IgA antinuclear autoantibodies, which were implicated in the development of IgA nephropathy. Our results indicate that Sle3 and Sle5 can independently complement with Sle1, through shared and unique mechanisms, to mediate the development of severe autoimmunity.

Indexed as

Genetic TestingAnimalsAutoantigensAutoimmunityB-LymphocytesCD8-Positive T-LymphocytesChromosomesImmunoglobulin GImmunoglobulin MLupus NephritisLymphocyte ActivationMiceMice, CongenicProtein Array AnalysisSplenomegalyAutoantigensImmunoglobulin GImmunoglobulin M

Identifiers

PMID17728789
OpenAlexW1981946587

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.