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

Autor:	Kapur R; Department of Experimental Immunohematology, Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;, Heitink-Pollé KM; Department of Pediatric Hematology-Oncology, University Medical Center Utrecht/Wilhelmina Children's Hospital, Utrecht, The Netherlands;, Porcelijn L; Department of Thrombocyte and Leukocyte Serology, Sanquin Diagnostic Services, Amsterdam, The Netherlands;, Bentlage AE; Department of Experimental Immunohematology, Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;, Bruin MC; Department of Pediatric Hematology-Oncology, University Medical Center Utrecht/Wilhelmina Children's Hospital, Utrecht, The Netherlands;, Visser R; Department of Experimental Immunohematology, Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;, Roos D; Department of Blood Cell Research, Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; and., Schasfoort RB; Medical Cell Biophysics, MIRA Institute, University of Twente, Enschede, The Netherlands., de Haas M; Department of Experimental Immunohematology, Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;, van der Schoot CE; Department of Experimental Immunohematology, Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;, Vidarsson G; Department of Experimental Immunohematology, Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;
Jazyk:	angličtina
Zdroj:	Blood [Blood] 2015 Mar 12; Vol. 125 (11), pp. 1793-802. Date of Electronic Publication: 2014 Dec 29.
DOI:	10.1182/blood-2014-05-579110
Abstrakt:	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. (© 2015 by The American Society of Hematology.)
Databáze:	MEDLINE
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