Evidence map›Paper›PMID 18467694›Full record

ArticleThe American journal of pathology2008

CD19 regulates skin and lung fibrosis via Toll-like receptor signaling in a model of bleomycin-induced scleroderma.

Ayumi Yoshizaki, Yohei Iwata, Kazuhiro Komura, Fumihide Ogawa, Toshihide Hara, Eiji Muroi, Motoi Takenaka, Kazuhiro Shimizu, Minoru Hasegawa, Manabu Fujimoto and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
9.3field-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

83 citing papers in PubMed, 204 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Occupation as a gendered-role and outcome in systemic sclerosis.Journal of scleroderma and related disorders · 2023
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

23 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.

Ayumi YoshizakiDepartment of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, 852-8501, Japan.
Yohei Iwata
Kazuhiro Komura
Fumihide Ogawa
Toshihide Hara
Eiji Muroi
Motoi Takenaka
Kazuhiro Shimizu
Minoru Hasegawa
Manabu Fujimoto
Thomas F Tedder
Shinichi Sato
Nagasaki University · JPKanazawa University · JPUniversity of Nagasaki · JPDuke Medical Center · US

Funding

Supplement - Inflammatory Triggers in B Cell AutoimmunityU19AI056363 · NIAID · DUKE UNIVERSITY · PI ST. CLAIR, EUGENE WILLIAM · 2003 to 2017
$35.3M
CD22 Regulation of B Lymphocyte Function and SurvivalR01CA096547 · NCI · DUKE UNIVERSITY · PI TEDDER, THOMAS F · 2003 to 2007
$1.3M
MS4A Family Members in Health and DiseaseR01CA105001 · NCI · DUKE UNIVERSITY · PI TEDDER, THOMAS F · 2004 to 2008
$1.2M
NCI NIH HHS CA105001NCI NIH HHS CA96547NCI NIH HHS R01 CA096547NCI NIH HHS R01 CA105001NIAID NIH HHS AI56363NIAID NIH HHS U19 AI056363
6 · The paper itself

Abstract

Mice subcutaneously injected with bleomycin, in an experimental model of human systemic sclerosis, develop cutaneous and lung fibrosis with autoantibody production. CD19 is a general "rheostat" that defines signaling thresholds critical for humoral immune responses, autoimmunity, and cytokine production. To determine the role of CD19 in the bleomycin-induced systemic sclerosis model, we investigated the development of fibrosis and autoimmunity in CD19-deficient mice. Bleomycin-treated wild-type mice exhibited dermal and lung fibrosis, hyper-gamma-globulinemia, autoantibody production, and enhanced serum and skin expression of various cytokines, including fibrogenic interleukin-4, interleukin-6, and transforming growth factor-beta1, all of which were inhibited by CD19 deficiency. Bleomycin treatment enhanced hyaluronan production in the skin, lung, and sera. Addition of hyaluronan, an endogenous ligand for Toll-like receptor (TLR) 2 and TLR4, stimulated B cells to produce various cytokines, primarily through TLR4; CD19 deficiency suppressed this stimulation. These results suggest that bleomycin induces fibrosis by enhancing hyaluronan production, which activates B cells to produce fibrogenic cytokines mainly via TLR4 and induce autoantibody production, and that CD19 deficiency suppresses fibrosis and autoantibody production by inhibiting TLR4 signals.

Indexed as

AnimalsAntigens, CD19AutoantibodiesBleomycinB-LymphocytesCytokinesFibrosisHyaluronic AcidMiceMice, KnockoutPulmonary FibrosisScleroderma, SystemicSignal TransductionSkinToll-Like Receptor 2Toll-Like Receptor 4Antigens, CD19AutoantibodiesBleomycinCytokinesHyaluronic AcidTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID18467694
PMCPMC2408424
OpenAlexW2054254671

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.