Evidence map›Paper›PMID 19201910›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Accelerated pathological and clinical nephritis in systemic lupus erythematosus-prone New Zealand Mixed 2328 mice doubly deficient in TNF receptor 1 and TNF receptor 2 via a Th17-associated pathway.

Noam Jacob, Haitao Yang, Luminita Pricop, Yi Liu, Xiaoni Gao, Song Guo Zheng, Juhua Wang, Hua-Xin Gao, Chaim Putterman, Michael N Koss and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Inhibition of B cell activation followingJournal of translational autoimmunity · 2021
    Article
  10. Review
  11. Review
  12. TNF-TNFR2 Signal Plays a Decisive Role in the Activation of CD4Advances in experimental medicine and biology · 2021
    Article
  13. Tregs in Autoimmune Uveitis.Advances in experimental medicine and biology · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. TLR7-Mediated Lupus Nephritis Is Independent of Type I IFN Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2018
    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

12 authors at 5 institutions in 1 country.

Noam JacobDepartment of Medicine, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA.
Haitao Yang
Luminita Pricop
Yi Liu
Xiaoni Gao
Song Guo Zheng
Juhua Wang
Hua-Xin Gao
Chaim Putterman
Michael N Koss
William Stohl
Chaim O Jacob
Center for Rheumatology · USHospital for Special Surgery · USAlbert Einstein College of Medicine · USCenter for Digestive and Liver Diseases · USUniversity of Southern California · US

Funding

Elucidation of novel gene variants predisposing to childhood and adult-onset SLER01AR057172 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JACOB, CHAIM O. · 2010 to 2014
$2.6M
Cytokine mechanisms in systemic lupus erythematosusR01AI057473 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JACOB, CHAIM O. · 2004 to 2008
$2.0M
The vital role of BAFF in the development of SLER01AR050193 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI STOHL, WILLIAM · 2006 to 2010
$1.7M
NIAID NIH HHS R01 AI057473NIAMS NIH HHS R01 AR050193NIAMS NIH HHS R01 AR057172NIDDK NIH HHS P30 DK04522
6 · The paper itself

Abstract

TNF-alpha has both proinflammatory and immunoregulatory functions. Whereas a protective role for TNF administration in systemic lupus erythematosus (SLE)-prone (New Zealand Black x New Zealand White)F(1) mice has been established, it remains uncertain whether this effect segregates at the individual TNFR. We generated SLE-prone New Zealand Mixed 2328 mice genetically deficient in TNFR1, in TNFR2, or in both receptors. Doubly-deficient mice developed accelerated pathological and clinical nephritis with elevated levels of circulating IgG anti-dsDNA autoantibodies and increased numbers of CD4(+) T lymphocytes, especially activated memory (CD44(high)CD62L(low)) CD4(+) T cells. We show that these cells expressed a Th17 gene profile, were positive for IL-17 intracellular staining by FACS, and produced exogenous IL-17 in culture. In contrast, immunological, pathological, and clinical profiles of mice deficient in either TNFR alone did not differ from those in each other or from those in wild-type controls. Thus, total ablation of TNF-alpha-mediated signaling was highly deleterious to the host in the New Zealand Mixed 2328 SLE model. These observations may have profound ramifications for the use of TNF and TNFR antagonists in human SLE and related autoimmune disorders, as well as demonstrate, for the first time, the association of the Th17 pathway with an animal model of SLE.

Indexed as

AnimalsAntibodies, AntinuclearCD4-Positive T-LymphocytesEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryFluorescent Antibody TechniqueGene Expression ProfilingInterleukin-17Lupus NephritisMiceMice, KnockoutReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIReverse Transcriptase Polymerase Chain ReactionT-Lymphocyte SubsetsAntibodies, AntinuclearInterleukin-17Receptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type II

Identifiers

PMID19201910
PMCPMC2790862
OpenAlexW1555057798

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.