Evidence map›Paper›PMID 26877251›Full record

ArticleCellular immunology2016

Strategies to target long-lived plasma cells for treating hemophilia A inhibitors.

Chao Lien Liu, Meghan J Lyle, Simon C Shin, Carol H Miao

Abstract read
In one paragraph

Article in Cellular immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. The changing face of immune tolerance induction in haemophilia A with the advent of emicizumab.Haemophilia : the official journal of the World Federation of Hemophilia · 2019
    Article
  10. Article
  11. Article
  12. Review
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 2 institutions in 2 countries.

Chao Lien LiuCenter for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA, USA; School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Meghan J LyleCenter for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA, USA.
Simon C ShinCenter for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA, USA.
Carol H MiaoCenter for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA, USA; Department of Pediatrics, University of Washington, Seattle, WA, USA. Electronic address: miao@u.washington.edu.
Taipei Medical University · TWUniversity of Washington · US

Funding

Non-viral Gene Medicine for the Treatment of HemophilaR01HL069049 · NHLBI · UNIVERSITY OF WASHINGTON · PI MIAO, CAROL H · 2003 to 2010
$3.9M
Direct in vivo bone marrow transfer of lentiviral vector to correct hemophilia AR01HL123326 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI MIAO, CAROL H · 2016 to 2019
$1.9M
Development of clinically feasible Ultrasound-mediated gene therapy for hemophiliaR01HL128139 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI MIAO, CAROL H · 2015 to 2018
$1.9M
NHLBI NIH HHS R01 HL069049NHLBI NIH HHS R01 HL123326NHLBI NIH HHS R01 HL128139NHLBI NIH HHS R01 HL69049
6 · The paper itself

Abstract

Long-lived plasma cells (LLPCs) can persistently produce anti-factor VIII (FVIII) antibodies which disrupt therapeutic effect of FVIII in hemophilia A patients with inhibitors. The migration of plasma cells to BM where they become LLPCs is largely controlled by an interaction between the chemokine ligand CXCL12 and its receptor CXCR4. AMD3100 combined with G-CSF inhibit their interactions, thus facilitating the mobilization of CD34(+) cells and blocking the homing of LLPCs. These reagents were combined with anti-CD20 to reduce B-cells and the specific IL-2/IL-2mAb (JES6-1) complexes to induce Treg expansion for targeting anti-FVIII immune responses. Groups of mice primed with FVIII plasmid and protein respectively were treated with the combined regimen for six weeks, and a significant reduction of anti-FVIII inhibitor titers was observed, associated with the dramatic decrease of circulating and bone marrow CXCR4(+) plasma cells. The combination regimens are highly promising in modulating pre-existing anti-FVIII antibodies in FVIII primed subjects.

Indexed as

AnimalsAntibodies, MonoclonalAntibodies, NeutralizingBenzylaminesCyclamsDisease Models, AnimalEnzyme-Linked Immunospot AssayFlow CytometryGranulocyte Colony-Stimulating FactorHemophilia AHeterocyclic CompoundsImmune ToleranceImmunosuppressive AgentsMicePlasma CellsReceptors, CXCR4Antibodies, MonoclonalAntibodies, NeutralizingBenzylaminesCXCR4 protein, mouseCyclamsGranulocyte Colony-Stimulating FactorHeterocyclic CompoundsImmunosuppressive AgentsplerixaforReceptors, CXCR4AMD3100Factor VIIIG-CSFHemophilia AImmune toleranceImmunomodulationInhibitorsPlasma cells

Identifiers

PMID26877251
PMCPMC4844017
OpenAlexW2274458465

What OpenQuestion holds

Textmetadata
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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.