Evidence map›Paper›PMID 19955422›Full record

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

IL-17-producing T cells can augment autoantibody-induced arthritis.

Jonathan P Jacobs, Hsin-Jung Wu, 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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Ssu72 Dual-Specific Protein Phosphatase: From Gene to Diseases.International journal of molecular sciences · 2021
    Review
  7. Article
  8. CD4European journal of immunology · 2020
    Article
  9. Review
  10. Targeting IgG in Arthritis: Disease Pathways and Therapeutic Avenues.International journal of molecular sciences · 2018
    Review
  11. Review
  12. Article
  13. Th17 in Animal Models of Rheumatoid Arthritis.Journal of clinical medicine · 2017
    Review
  14. Arthritis models: usefulness and interpretation.Seminars in immunopathology · 2017
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Tetramers reveal IL-17-secreting CD4+ T cells that are specific for U1-70 in lupus and mixed connective tissue disease.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

4 authors at 1 institution in 1 country.

Jonathan P JacobsDepartment of Pathology, Harvard Medical School, Boston, MA 02115, USA.
Hsin-Jung Wu
Christophe Benoist
Diane Mathis
Harvard University · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
Post-transcriptional regulation of inflammatory arthritisP01AI065858 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI ANDERSON, PAUL J. · 2006 to 2010
$11.1M
ARTHRITOGENIC IGS--WHAT ARE THEY? WHY ARE THEY MADE?R01AR046580 · NIAMS · JOSLIN DIABETES CENTER · PI MATHIS, DIANE J · 2000 to 2009
$3.8M
Genetics of arthritis suscuptibility in outbred HS miceR01AR055271 · NIAMS · JOSLIN DIABETES CENTER · PI BENOIST, CHRISTOPHE O. · 2007 to 2011
$1.8M
Howard Hughes Medical InstituteNIAID NIH HHS P01 AI065858NIAMS NIH HHS R01 AR046580NIAMS NIH HHS R01 AR055271NIDDK NIH HHS P30 DK036836NIDDK NIH HHS P30 DK36836
6 · The paper itself

Abstract

Rheumatoid arthritis is a T lymphocyte-mediated disorder, but the precise nature of T cell involvement remains unclear. In the K/BxN mouse model of inflammatory arthritis, T cells initiate disease by providing help to B cells to produce arthritogenic autoantibodies. Here, we have characterized an additional, nonhumoral role for T cells in promoting autoantibody-induced arthritis. Autoreactive KRN T cells introduced either by direct transfer or bone marrow transplantation into B-cell-deficient hosts enhanced K/BxN serum-transferred arthritis, an effect that was dependent on expression of the cognate MHC-molecule/peptide complex. The T cell influence was dependent on interleukin (IL)-17; in contrast, standard serum-transferred arthritis, unenhanced by the addition of T cells, was unaffected by IL-17 neutralization. An IL-17-producing population of transferred KRN T cells was identified and found to be supported by the cotransfer of arthritogenic autoantibodies. IL-17-producing KRN T cells were enriched in inflamed joints of K/BxN mice, suggesting either selective recruitment or preferential differentiation. These results demonstrate the potential for autoreactive T cells to play two roles in the development of arthritis, both driving the production of pathogenic autoantibodies and bolstering the subsequent inflammatory cascade dependent on the innate immune system.

Indexed as

AnimalsArthritisAutoantibodiesBloodCell DifferentiationInterleukin-17MiceMice, TransgenicNeutralization TestsT-LymphocytesAutoantibodiesInterleukin-17

Identifiers

PMID19955422
PMCPMC2799826
OpenAlexW2150193383

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.