Domain I of beta 2GPI is capable of blocking serum IgA antiphospholipid antibodies binding in vitro: an effect enhanced by PEGylation
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Published version
OA Location
Author(s)
Type
Journal Article
Abstract
Objectives
This study aims to inhibit antiphospholipid syndrome (APS) serum derived IgA anti-beta-2-glycoprotein I (aβ2GPI) binding using Domain I (DI).
Methods
Serum from 13 APS patients was tested for IgA aβ2GPI and Anti-Domain I. Whole IgA was purified by peptide M affinity chromatography from positive serum samples. Serum was tested for IgA aβ2GPI binding in the presence and absence of either DI or of two biochemically modified variants containing either 20 kDa of poly(ethylene glycol) (PEG) or 40 kDa of PEG.
Results
Significant inhibition with DI was possible with average inhibition of 23% (N = 13). Further inhibitions using 20 kDa PEG-DI and 40 kDa PEG-DI variants showed significant inhibition (p = 0.0001) with both the 40 kDa PEG-DI and 20 kDa PEG-DI variants showing increased inhibition compared with DI alone (p = 0.0001 and p = 0.001, n = 10).
Conclusions
Inhibition of IgA aβ2GPI by DI is possible and can be enhanced by biochemical modification in a subset of patients.
This study aims to inhibit antiphospholipid syndrome (APS) serum derived IgA anti-beta-2-glycoprotein I (aβ2GPI) binding using Domain I (DI).
Methods
Serum from 13 APS patients was tested for IgA aβ2GPI and Anti-Domain I. Whole IgA was purified by peptide M affinity chromatography from positive serum samples. Serum was tested for IgA aβ2GPI binding in the presence and absence of either DI or of two biochemically modified variants containing either 20 kDa of poly(ethylene glycol) (PEG) or 40 kDa of PEG.
Results
Significant inhibition with DI was possible with average inhibition of 23% (N = 13). Further inhibitions using 20 kDa PEG-DI and 40 kDa PEG-DI variants showed significant inhibition (p = 0.0001) with both the 40 kDa PEG-DI and 20 kDa PEG-DI variants showing increased inhibition compared with DI alone (p = 0.0001 and p = 0.001, n = 10).
Conclusions
Inhibition of IgA aβ2GPI by DI is possible and can be enhanced by biochemical modification in a subset of patients.
Date Issued
2019-06-01
Date Acceptance
2019-04-25
Citation
Lupus, 2019, 28 (7), pp.893-897
ISSN
1477-0962
Publisher
SAGE Publications
Start Page
893
End Page
897
Journal / Book Title
Lupus
Volume
28
Issue
7
Copyright Statement
© 2019 The Author(s). Article reuse guidelines: sagepub.com/journals-permissions. CC BY (https://creativecommons.org/licenses/by/4.0/).
Sponsor
Arthritis Research UK
Identifier
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000471342500012&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
Grant Number
21223
Subjects
Science & Technology
Life Sciences & Biomedicine
Rheumatology
Antiphospholipid syndrome
Domain I
PEGylation
IMMUNE-COMPLEXES
THROMBOSIS
DIAGNOSIS
Publication Status
Published
Date Publish Online
2019-05-24