Cleavage of anti-PF4/heparin IgG by a bacterial protease and potential benefit in heparin-induced thrombocytopenia.
Animals
Bacterial Proteins
/ pharmacology
Fibrin
/ genetics
Heparin
/ administration & dosage
Humans
Immunoglobulin G
/ metabolism
Mice, Transgenic
Microfluidic Analytical Techniques
Platelet Aggregation
/ drug effects
Platelet Factor 4
/ metabolism
Receptors, IgG
/ metabolism
Streptococcus pyogenes
/ enzymology
Thrombocytopenia
/ chemically induced
Journal
Blood
ISSN: 1528-0020
Titre abrégé: Blood
Pays: United States
ID NLM: 7603509
Informations de publication
Date de publication:
30 05 2019
30 05 2019
Historique:
received:
16
10
2018
accepted:
25
03
2019
pubmed:
29
3
2019
medline:
24
12
2019
entrez:
29
3
2019
Statut:
ppublish
Résumé
Heparin-induced thrombocytopenia (HIT) is due to immunoglobulin G (IgG) antibodies, which bind platelet factor 4 (PF4) modified by polyanions, such as heparin (H). IgG/PF4/polyanion complexes directly activate platelets via Fc gamma type 2 receptor A (FcγRIIA) receptors. A bacterial protease, IgG-degrading enzyme of
Identifiants
pubmed: 30917957
pii: S0006-4971(20)42520-0
doi: 10.1182/blood.2019000437
doi:
Substances chimiques
Bacterial Proteins
0
FCGR2A protein, human
0
Immunoglobulin G
0
Mac-1-like protein, Streptococcus
0
Receptors, IgG
0
Platelet Factor 4
37270-94-3
Fibrin
9001-31-4
Heparin
9005-49-6
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2427-2435Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2019 by The American Society of Hematology.