Current Anti-HPA-1a Standard Antibodies React with the β3 Integrin Subunit but not with αIIbβ3 and αvβ3 Complexes.


Journal

Thrombosis and haemostasis
ISSN: 2567-689X
Titre abrégé: Thromb Haemost
Pays: Germany
ID NLM: 7608063

Informations de publication

Date de publication:
Nov 2019
Historique:
pubmed: 7 10 2019
medline: 9 4 2020
entrez: 7 10 2019
Statut: ppublish

Résumé

 Fetal/neonatal alloimmune thrombocytopenia (FNAIT) results from maternal alloantibodies (abs) reacting with fetal platelets expressing paternal human platelet antigens (HPAs), mostly HPA-1a. Anti-HPA-1a abs, are the most frequent cause of severe thrombocytopenia and intracranial hemorrhage (ICH).  Titration of anti-HPA-1a in maternal serum using standard National Institute for Biological Standards and Control (NIBSC) 03/152 is one diagnostic approach to predict the severity of FNAIT. Recently, we found three anti-HPA-1a subtypes reacting with the β3 subunit independently or dependently from complexes with αIIb and αv. Endothelial cell-reactive anti-αvβ3 abs were found predominantly in cases with ICH. Our aim was to assess whether available standard material represents all anti-HPA-1a subtypes.  In this study, anti-HPA-1a sera (NIBSC 03/152) and human monoclonal antibodies (moabs) against HPA-1a (moabs 26.4 and 813) were evaluated using transfected cell lines expressing αIIbβ3, αvβ3 or monomeric cβ3.  Flow cytometry analyses with well-characterized murine moabs recognizing αIIbβ3, αvβ3, or β3 alone demonstrated that AP3 reacts compound-independently, whereas compound-dependent moabs Gi5 and 23C6 reacted only with complexes. NIBSC 03/152, moabs 26.4, and 813 against HPA-1a reacted like AP3, same results were obtained with monomeric cβ3 in immunoblotting. Antigen capture assay targeting endothelial cells showed anti-HPA-1a reactivity disappearance after cβ3 beads adsorption. Furthermore, in contrast to anti-HPA-1a abs from ICH cases, none of NIBSC 03/152, 26.4, and 813 inhibited tube formation.  These results suggest that current anti-HPA-1a standard material contains only the anti-β3 subtype. The absence of anti-αvβ3 makes NIBSC 03/152 less suitable as standard to predict the severity of FNAIT.

Sections du résumé

BACKGROUND BACKGROUND
 Fetal/neonatal alloimmune thrombocytopenia (FNAIT) results from maternal alloantibodies (abs) reacting with fetal platelets expressing paternal human platelet antigens (HPAs), mostly HPA-1a. Anti-HPA-1a abs, are the most frequent cause of severe thrombocytopenia and intracranial hemorrhage (ICH).
OBJECTIVES OBJECTIVE
 Titration of anti-HPA-1a in maternal serum using standard National Institute for Biological Standards and Control (NIBSC) 03/152 is one diagnostic approach to predict the severity of FNAIT. Recently, we found three anti-HPA-1a subtypes reacting with the β3 subunit independently or dependently from complexes with αIIb and αv. Endothelial cell-reactive anti-αvβ3 abs were found predominantly in cases with ICH. Our aim was to assess whether available standard material represents all anti-HPA-1a subtypes.
MATERIALS AND METHODS METHODS
 In this study, anti-HPA-1a sera (NIBSC 03/152) and human monoclonal antibodies (moabs) against HPA-1a (moabs 26.4 and 813) were evaluated using transfected cell lines expressing αIIbβ3, αvβ3 or monomeric cβ3.
RESULTS RESULTS
 Flow cytometry analyses with well-characterized murine moabs recognizing αIIbβ3, αvβ3, or β3 alone demonstrated that AP3 reacts compound-independently, whereas compound-dependent moabs Gi5 and 23C6 reacted only with complexes. NIBSC 03/152, moabs 26.4, and 813 against HPA-1a reacted like AP3, same results were obtained with monomeric cβ3 in immunoblotting. Antigen capture assay targeting endothelial cells showed anti-HPA-1a reactivity disappearance after cβ3 beads adsorption. Furthermore, in contrast to anti-HPA-1a abs from ICH cases, none of NIBSC 03/152, 26.4, and 813 inhibited tube formation.
CONCLUSION CONCLUSIONS
 These results suggest that current anti-HPA-1a standard material contains only the anti-β3 subtype. The absence of anti-αvβ3 makes NIBSC 03/152 less suitable as standard to predict the severity of FNAIT.

Identifiants

pubmed: 31587244
doi: 10.1055/s-0039-1696716
pmc: PMC6827430
mid: NIHMS1054854
doi:

Substances chimiques

Antibodies, Monoclonal 0
Antigens, Human Platelet 0
ITGB3 protein, human 0
Integrin alphaVbeta3 0
Integrin beta3 0
Isoantibodies 0
Platelet Glycoprotein GPIIb-IIIa Complex 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1807-1815

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL131836
Pays : United States

Informations de copyright

Georg Thieme Verlag KG Stuttgart · New York.

Déclaration de conflit d'intérêts

None declared.

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Auteurs

Behnaz Bayat (B)

Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Giessen, Germany.

Annalena Traum (A)

Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Giessen, Germany.

Heike Berghöfer (H)

Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Giessen, Germany.

Silke Werth (S)

Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Giessen, Germany.

Jieging Zhu (J)

Blood Research Institute, Milwaukee, Wisconsin, United States.

Gregor Bein (G)

Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Giessen, Germany.

Ulrich J Sachs (UJ)

Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Giessen, Germany.
Center for Transfusion Medicine and Hemotherapy, University Hospital Marburg, Marburg, Germany.

Sentot Santoso (S)

Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Giessen, Germany.

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Classifications MeSH