Evidence map›Paper›PMID 23150717›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

B cell TLR7 expression drives anti-RNA autoantibody production and exacerbates disease in systemic lupus erythematosus-prone mice.

Sun-Hee Hwang, Huiyin Lee, Miwako Yamamoto, Leigh A Jones, Jivanaah Dayalan, Richard Hopkins, Xin J Zhou, Felix Yarovinsky, John E Connolly, Maria A Curotto de Lafaille and 2 more

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

77 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Frontiers in immunology · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Potential of mRNA vaccines to become versatile cancer vaccines.World journal of clinical oncology · 2022
    Review
  16. Review
  17. Article
  18. Immunogenicity ofAccounts of chemical research · 2021
    Review
  19. Review
  20. The dynamic epigenetic regulation of the inactive X chromosome in healthy human B cells is dysregulated in lupus patients.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article

17 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

12 authors at 4 institutions in 2 countries.

Sun-Hee HwangDepartment of Immunology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.
Huiyin Lee
Miwako Yamamoto
Leigh A Jones
Jivanaah Dayalan
Richard Hopkins
Xin J Zhou
Felix Yarovinsky
John E Connolly
Maria A Curotto de Lafaille
Edward K Wakeland
Anna-Marie Fairhurst
Singapore Immunology Network · SGThe University of Texas Southwestern Medical Center · USBaylor University · USBaylor University Medical Center · US

Funding

Genetic Pathways Contributing to Systemic Lupus Erythematosus PathogenesisR37AI045196 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI WAKELAND, EDWARD K. · 2003 to 2012
$4.0M
Defining genetic pathways to severe systemic autoimmunityR01AI069371 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI WAKELAND, EDWARD K. · 2006 to 2010
$2.9M
Cellular and molecular mechanisms of host resistance to Toxoplasma gondiiR01AI085263 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI YAROVINSKY, FELIX · 2010 to 2014
$1.9M
GENETIC PATHWAYS CONTRIBUTING TO SLE PATHOGENESISR01AI045196 · NIAID · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI WAKELAND, EDWARD K · 1998 to 2002
$1.1M
NIAID NIH HHS R01 AI045196NIAID NIH HHS R01 AI069371NIAID NIH HHS R01 AI085263NIAID NIH HHS R37 AI045196
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterized by the production of antinuclear autoantibodies. Antinuclear autoantibody development is recognized as one of the initial stages of disease that often results in systemic inflammation, kidney disease, and death. The etiology is complex, but it is clear that innate pathways may play an important role in disease progression. Recent data have highlighted an important role for the TLR family, particularly TLR7, in both human disease and murine models. In this study, we have presented a low copy conditional TLR7 transgenic (Tg7) mouse strain that does not develop spontaneous autoimmunity. When we combine Tg7 with the Sle1 lupus susceptibility locus, the mice develop severe disease. Using the CD19(Cre) recombinase system, we normalized expression of TLR7 solely within the B cells. Using this method we demonstrated that overexpression of TLR7 within the B cell compartment reduces the marginal zone B cell compartment and increases B and T cell activation but not T follicular helper cell development. Moreover, this enhanced B cell TLR7 expression permits the specific development of Abs to RNA/protein complexes and exacerbates SLE disease.

Indexed as

Genetic Predisposition to DiseaseAnimalsAutoantibodiesB-Lymphocyte SubsetsDisease ProgressionEpistasis, GeneticFemaleGene Expression Regulation, DevelopmentalHumansLupus Erythematosus, SystemicMaleMembrane GlycoproteinsMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicAutoantibodiesMembrane GlycoproteinsMultiprotein ComplexesTlr7 protein, mouseToll-Like Receptor 7

Identifiers

PMID23150717
PMCPMC3544945
OpenAlexW2164736950

What OpenQuestion holds

Textmetadata
LicenceTDM
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.