Evidence map›Paper›PMID 17536017›Full record

ArticleBlood2007

Tissue factor: a link between C5a and neutrophil activation in antiphospholipid antibody induced fetal injury.

Patricia Redecha, Rachel Tilley, Michael Tencati, Jane E Salmon, Daniel Kirchhofer, Nigel Mackman, Guillermina Girardi

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03152058 (Certolizumab to Prevent Pregnancy Complications in High-Risk Patients With APS or SLE -), which is not on this map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
11.6field-weighted citation impact, top 1% 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.

NCT03152058 phase2recruitingnot on this mapstarted 2017, after this paper: background citation

Certolizumab to Prevent Pregnancy Complications in High-Risk Patients With APS or SLE - (IMPACT Study: IMProve Pregnancy in APS With Certolizumab Therapy)

TypeinterventionalSponsorDavid Ware BranchRan2017 to 2027Enrolled55ConditionsHigh Risk Pregnancy, Pregnancy Complications, Antiphospholipid Syndrome in Pregnancy, Lupus Anticoagulant DisorderArmsCertolizumab Pegol
3 · Its place in the literature

Who cites it

116 citing papers in PubMed, 1 synthesis or guideline pooled it, 290 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Observational
  8. Article
  9. Review
  10. Review
  11. The complement system in autoimmune diseases: pathogenesis, diagnostic markers, and therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  12. Review
  13. How We Interpret Thrombosis with Thrombocytopenia Syndrome?International journal of molecular sciences · 2024
    Review
  14. Review
  15. Article
  16. The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023
    Review
  17. Article
  18. Review
  19. The complement system and autoimmune diseases.Chronic diseases and translational medicine · 2022
    Review
  20. Pathophysiology of Antiphospholipid Syndrome.Thrombosis and haemostasis · 2022
    Article

56 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

7 authors at 3 institutions in 1 country.

Patricia RedechaHospital for Special Surgery, Department of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.
Rachel Tilley
Michael Tencati
Jane E Salmon
Daniel Kirchhofer
Nigel Mackman
Guillermina Girardi
Scripps Research Institute · USHospital for Special Surgery · USCornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fetal loss in patients with antiphospholipid (aPL) antibodies has been ascribed to thrombosis of placental vessels. However, we have shown that inflammation, specifically activation of complement with generation of the anaphylotoxin C5a, is an essential trigger of fetal injury. In this study, we analyzed the role of the procoagulant molecule tissue factor (TF) in a mouse model of aPL antibody-induced pregnancy loss. We found that either blockade of TF with a monoclonal antibody in wild-type mice or a genetic reduction of TF prevented aPL antibody-induced inflammation and pregnancy loss. In response to aPL antibody-generated C5a, neutrophils express TF potentiating inflammation in the deciduas and leading to miscarriages. Importantly, we showed that TF in myeloid cells but not fetal-derived cells (trophoblasts) was associated with fetal injury, suggesting that the site for pathologic TF expression is neutrophils. We found that TF expression in neutrophils contributes to respiratory burst and subsequent trophoblast injury and pregnancy loss induced by aPL antibodies. The identification of TF as an important mediator of C5a-induced oxidative burst in neutrophils in aPL-induced fetal injury provides a new target for therapy to prevent pregnancy loss in the antiphospholipid syndrome.

Indexed as

AnimalsAntibodies, AntiphospholipidComplement C5aEmbryo LossFemaleHumansMiceNeutrophil ActivationNeutrophilsOxidative StressPregnancyPrenatal InjuriesReceptor, Anaphylatoxin C5aSignal TransductionThromboplastinAntibodies, AntiphospholipidComplement C5aReceptor, Anaphylatoxin C5aThromboplastin

Identifiers

PMID17536017
PMCPMC1988945
OpenAlexW2044707852

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.