Evidence map›Paper›PMID 30405613›Full record

ArticleFrontiers in immunology2018

PEGylated Domain I of Beta-2-Glycoprotein I Inhibits the Binding, Coagulopathic, and Thrombogenic Properties of IgG From Patients With the Antiphospholipid Syndrome.

Thomas C R McDonnell, Rohan Willis, Charis Pericleous, Vera M Ripoll, Ian P Giles, David A Isenberg, Allan R Brasier, Emilio B Gonzalez, Elizabeth Papalardo, Zurina Romay-Penabad and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Thomas C R McDonnellDivision of Medicine, Centre for Rheumatology Research, University College London, London, United Kingdom.
Rohan WillisInternal Medicine, University of Texas Medical Branch, Galveston, TX, United States.
Charis PericleousDivision of Medicine, Centre for Rheumatology Research, University College London, London, United Kingdom.
Vera M RipollDivision of Medicine, Centre for Rheumatology Research, University College London, London, United Kingdom.
Ian P GilesDivision of Medicine, Centre for Rheumatology Research, University College London, London, United Kingdom.
David A IsenbergDivision of Medicine, Centre for Rheumatology Research, University College London, London, United Kingdom.
Allan R BrasierInternal Medicine, University of Texas Medical Branch, Galveston, TX, United States.
Emilio B GonzalezInternal Medicine, University of Texas Medical Branch, Galveston, TX, United States.
Elizabeth PapalardoInternal Medicine, University of Texas Medical Branch, Galveston, TX, United States.
Zurina Romay-PenabadInternal Medicine, University of Texas Medical Branch, Galveston, TX, United States.
Mohammad JamaluddinInternal Medicine, University of Texas Medical Branch, Galveston, TX, United States.
Yiannis IoannouDivision of Medicine, Centre for Rheumatology Research, University College London, London, United Kingdom.
Anisur RahmanDivision of Medicine, Centre for Rheumatology Research, University College London, London, United Kingdom.
The University of Texas Medical Branch at Galveston · USUniversity College London · GBGreat Ormond Street Hospital · GB

Funding

UTMB Clinical and Translational Science AwardUL1TR001439 · NCATS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI URBAN, RANDALL J · 2015 to 2024
$40.0M
Antiphospholipid antibodies and lupus: new molecular targets for treatmentR01AR056745 · NIAMS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BRASIER, ALLAN R., GONZALEZ, EMILIO B · 2010 to 2014
$1.6M
Medical Research Council MR/P017371/1NCATS NIH HHS UL1 TR001439NIAMS NIH HHS R01 AR056745
6 · The paper itself

Abstract

APS is an autoimmune disease in which antiphospholipid antibodies (aPL) cause vascular thrombosis and pregnancy morbidity. In patients with APS, aPL exert pathogenic actions by binding serum beta-2-glycoprotein I (β2GPI) via its N-terminal domain I (DI). We previously showed that bacterially-expressed recombinant DI inhibits biological actions of IgG derived from serum of patients with APS (APS-IgG). DI is too small (7 kDa) to be a viable therapeutic agent. Addition of polyethylene glycol (PEGylation) to small molecules enhances the serum half-life, reduces proteolytic targeting and can decrease immunogenicity. It is a common method of tailoring pharmacokinetic parameters and has been used in the production of many therapies in the clinic. However, PEGylation of molecules may reduce their biological activity, and the size of the PEG group can alter the balance between activity and half-life extension. Here we achieve production of site-specific PEGylation of recombinant DI (PEG-DI) and describe the activities

Indexed as

Blood CoagulationProtein Interaction Domains and MotifsAdultAnimalsAntibodies, AntiphospholipidAntiphospholipid Syndromebeta 2-Glycoprotein IDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleHumansImmunoglobulin GMaleMiceMiddle AgedProtein BindingAntibodies, Antiphospholipidbeta 2-Glycoprotein IImmunoglobulin Gantiphospholipid syndromebiologicsdomain IPEGylationtherapeutics

Identifiers

PMID30405613
PMCPMC6204385
OpenAlexW2894465451

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.