C-reactive protein enhances IgG-mediated phagocyte responses and thrombocytopenia.

Abstract:

:Immune-mediated platelet destruction is most frequently caused by allo- or autoantibodies via Fcγ receptor-dependent phagocytosis. Disease severity can be predicted neither by antibody isotype nor by titer, indicating that other factors play a role. Here we show that the acute phase protein C-reactive protein (CRP), a ligand for Fc receptors on phagocytes, enhances antibody-mediated platelet destruction by human phagocytes in vitro and in vivo in mice. Without antiplatelet antibodies, CRP was found to be inert toward platelets, but it bound to phosphorylcholine exposed after oxidation triggered by antiplatelet antibodies, thereby enhancing platelet phagocytosis. CRP levels were significantly elevated in patients with allo- and autoantibody-mediated thrombocytopenias compared with healthy controls. Within a week, intravenous immunoglobulin treatment in children with newly diagnosed immune thrombocytopenia led to significant decrease of CRP levels, increased platelet numbers, and clinically decreased bleeding severity. Furthermore, the higher the level of CRP at diagnosis, the longer it took before stable platelet counts were reached. These data suggest that CRP amplifies antibody-mediated platelet destruction and may in part explain the aggravation of thrombocytopenia on infections. Hence, targeting CRP could offer new therapeutic opportunities for these patients.

journal_name

Blood

journal_title

Blood

authors

Kapur R,Heitink-Pollé KM,Porcelijn L,Bentlage AE,Bruin MC,Visser R,Roos D,Schasfoort RB,de Haas M,van der Schoot CE,Vidarsson G

doi

10.1182/blood-2014-05-579110

subject

Has Abstract

pub_date

2015-03-12 00:00:00

pages

1793-802

issue

11

eissn

0006-4971

issn

1528-0020

pii

blood-2014-05-579110

journal_volume

125

pub_type

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