Evidence map›Paper›PMID 23696725›Full record

ArticlePLoS computational biology2013

Polymorphisms in the F8 gene and MHC-II variants as risk factors for the development of inhibitory anti-factor VIII antibodies during the treatment of hemophilia a: a computational assessment.

Gouri Shankar Pandey, Chen Yanover, Tom E Howard, Zuben E Sauna

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Reducing Immunogenicity by Design: Approaches to Minimize Immunogenicity of Monoclonal Antibodies.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. 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 3 institutions in 1 country.

Gouri Shankar PandeyLaboratory of Hemostasis, Division of Hematology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, USA.
Chen Yanover
Tom E Howard
Zuben E Sauna
Center for Biologics Evaluation and Research · USFred Hutch Cancer Center · USVA Greater Los Angeles Healthcare System · US

Funding

Mechanisms of Race-Based Differences in Factor VIII Immunogenicity in HemophiliaRC2HL101851 · NHLBI · SEPULVEDA RESEARCH CORPORATION · PI HOWARD, TOM EUGENE, PRATT, KATHLEEN PALMER · 2009 to 2010
$6.5M
Genetic Variation in Factor IX and Thrombosis RiskR01HL072533 · NHLBI · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI ALMASY, LAURA A. · 2003 to 2006
$1.5M
Genetic Variation in Factor IX and Thrombosis RiskK08HL071130 · NHLBI · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI HOWARD, TOM E. · 2002 to 2006
$634k
NHLBI NIH HHS 1RC2-HL101851NHLBI NIH HHS HL-71130NHLBI NIH HHS HL-72533NHLBI NIH HHS K08 HL071130NHLBI NIH HHS R01 HL072533NHLBI NIH HHS RC2 HL101851
6 · The paper itself

Abstract

The development of neutralizing anti-drug-antibodies to the Factor VIII protein-therapeutic is currently the most significant impediment to the effective management of hemophilia A. Common non-synonymous single nucleotide polymorphisms (ns-SNPs) in the F8 gene occur as six haplotypes in the human population (denoted H1 to H6) of which H3 and H4 have been associated with an increased risk of developing anti-drug antibodies. There is evidence that CD4+ T-cell response is essential for the development of anti-drug antibodies and such a response requires the presentation of the peptides by the MHC-class-II (MHC-II) molecules of the patient. We measured the binding and half-life of peptide-MHC-II complexes using synthetic peptides from regions of the Factor VIII protein where ns-SNPs occur and showed that these wild type peptides form stable complexes with six common MHC-II alleles, representing 46.5% of the North American population. Next, we compared the affinities computed by NetMHCIIpan, a neural network-based algorithm for MHC-II peptide binding prediction, to the experimentally measured values and concluded that these are in good agreement (area under the ROC-curve of 0.778 to 0.972 for the six MHC-II variants). Using a computational binding predictor, we were able to expand our analysis to (a) include all wild type peptides spanning each polymorphic position; and (b) consider more MHC-II variants, thus allowing for a better estimation of the risk for clinical manifestation of anti-drug antibodies in the entire population (or a specific sub-population). Analysis of these computational data confirmed that peptides which have the wild type sequence at positions where the polymorphisms associated with haplotypes H3, H4 and H5 occur bind MHC-II proteins significantly more than a negative control. Taken together, the experimental and computational results suggest that wild type peptides from polymorphic regions of FVIII constitute potential T-cell epitopes and thus could explain the increased incidence of anti-drug antibodies in hemophilia A patients with haplotypes H3 and H4.

Indexed as

Amino Acid SequenceAntibodiesBlack PeopleComputational BiologyFactor VIIIHaplotypesHemophilia AHistocompatibility Antigens Class IIHumansMolecular Sequence DataPeptide FragmentsPolymorphism, Single NucleotideProtein BindingRisk FactorsAntibodiesFactor VIIIHistocompatibility Antigens Class IIPeptide Fragments

Identifiers

PMID23696725
PMCPMC3656107
OpenAlexW2005424812

What OpenQuestion holds

Textmetadata
LicenceCC0
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.