Evidence map›Paper›PMID 19805369›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

The same systemic autoimmune disease provokes arthritis and endocarditis via distinct mechanisms.

Bryce A Binstadt, Jennifer L Hebert, Adriana Ortiz-Lopez, Roderick Bronson, Christophe Benoist, Diane Mathis

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.0field-weighted citation impact, top 24% 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, 42 citations in OpenAlex.

  1. Immune Mechanisms of Heart Valve Development, Homeostasis, and Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Profibrotic VEGFR3-Dependent Lymphatic Vessel Growth in Autoimmune Valvular Carditis.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Article
  9. Autoimmune Valvular Carditis Requires Endothelial Cell TNFR1 Expression.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Article
  10. Article
  11. Article
  12. Annexin A1 attenuates cardiac diastolic dysfunction in mice with inflammatory arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  13. Review
  14. Article
  15. Review
  16. Triggers of Inflammatory Heart Disease.Frontiers in cell and developmental biology · 2020
    Review
  17. Heart Inflammation: Immune Cell Roles and Roads to the Heart.The American journal of pathology · 2019
    Review
  18. Article
  19. Review
  20. CD301b/MGL2Circulation · 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

6 authors at 2 institutions in 1 country.

Bryce A BinstadtSection on Immunology and Immunogenetics, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA. binstadt@umn.edu
Jennifer L Hebert
Adriana Ortiz-Lopez
Roderick Bronson
Christophe Benoist
Diane Mathis
Harvard University · USUniversity of Minnesota · US

Funding

ARTHRITOGENIC IGS--WHAT ARE THEY? WHY ARE THEY MADE?R01AR046580 · NIAMS · JOSLIN DIABETES CENTER · PI MATHIS, DIANE J · 2000 to 2009
$3.8M
Characterization of a New Mouse Model of Autoimmune Cardiac Valve DiseaseK08AR054317 · NIAMS · UNIVERSITY OF MINNESOTA · PI BINSTADT, BRYCE · 2007 to 2011
$644k
NIAMS NIH HHS K08 AR 054317NIAMS NIH HHS K08 AR054317NIAMS NIH HHS R01 AR 046580NIAMS NIH HHS R01 AR046580
6 · The paper itself

Abstract

The immune mechanisms that provoke concomitant inflammation of synovial joints and cardiac valves in disorders such as rheumatic fever and systemic lupus erythematosus remain poorly defined. Here, we report the discovery of spontaneous endocarditis-in addition to their well-studied autoimmune arthritis-in K/BxN T cell receptor (TCR) transgenic mice. The same adaptive immune system elements were required for initiation of arthritis and endocarditis, and both diseases were dependent on autoantibodies. In contrast, the participation of key innate immune system molecules and perhaps T cells as effectors of inflammation differed between the 2 target tissues. Arthritis in K/BxN TCR transgenic mice depended primarily on complement C5 and not FcRgamma-using receptors; conversely, endocarditis depended essentially on FcRgamma receptors and not C5. Elucidating how a single systemic autoimmune disease engages distinct immune effector pathways to damage different target tissues is essential for optimizing the treatment of such disorders.

Indexed as

AnimalsArthritisAutoantibodiesAutoimmune DiseasesDisease Models, AnimalEndocarditisMiceMice, TransgenicAutoantibodies

Identifiers

PMID19805369
PMCPMC2757808
OpenAlexW2116953305

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.