Kinetics of platelets in dogs with thrombocytopenia induced by antiglycoprotein IIb/IIIa receptor monoclonal antibody

Hosono, Makoto; Sone, Naoaki; Endo, Keigo; Saga, Tsuneo; Kobayashi, Hisataka; Hosono, Masamichi; Sakahara, Harumi; Yasunaga, Kōjirō; Konishi, Junji

doi:10.1016/0969-8051(94)00072-r

Cited by 8 publications

(4 citation statements)

References 15 publications

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“…Any increase in liver radioactivity, with a parallel decline in blood radioactivity, can thus be attributed to the deposition of 111 In-labelled platelets in this organ. These findings differ from the results published in a study with an IgG 2 antibody on dog platelets (22). The authors described a permanent uptake of platelets by the liver, but they monitored the changes in organ radioactivity for only 6 h after the injection of the antibody.…”

Section: Discussioncontrasting

confidence: 97%

“…The present study confirms that certain anti-platelet antibodies cause acute thrombocytopenia of varying degrees of severity. Other studies have also shown the development of acute thrombocytopenia after injection of IgG 2 anti-platelet antibodies in both dogs and apes (22,37). Binding of anti-platelet antibodies to their specific antigens on the platelet surface appears to be a prerequisite for the development of thrombocytopenia since the non-binding antibody did not have any effect on the platelet count.…”

Section: Discussionmentioning

confidence: 91%

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The Effect of Monoclonal Anti-human-platelet Antibodies on Platelet Kinetics in a Baboon Model: IgG Subclass Dependency

Coetzee

Pieters²,

Wyk³

et al. 2000

Thromb Haemost

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SummaryWe assessed the in vivo effect of six intact anti-human antiplatelet antibodies of two major IgG subclasses on platelet kinetics in baboons. Five of the six antibodies tested caused thrombocytopenia of varying degree when injected at a precalculated threshold value. An agglutinating IgG1 antibody (MA-8L4A12) caused a long-lasting, mild thrombocytopenia with a predominant uptake of radiolabelled platelets in the spleen, while the four IgG2 antibodies tested (MA-13G8E1, MA-2M5A6, MA-21K2E8 and MA-22M10) caused a severe, transient thrombocytopenia with uptake of platelets in the liver. Two of the IgG2 antibodies (MA-13G8E1 and MA-2M5A6) caused platelet activation and aggregation in vitro, whilst the other two did not elicit a platelet aggregation response. The platelet survival time was shortened with all five of the thrombocytopenia-inducing antibodies, while only one antibody (MA-2M5A6) had a significant effect on the bleeding time. This study indicates that the IgG subclasss may be a determining factor in the outcome of platelet sequestration in immune-induced thrombocytopenia.

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Section: Discussioncontrasting

confidence: 97%

Section: Discussionmentioning

confidence: 91%

The Effect of Monoclonal Anti-human-platelet Antibodies on Platelet Kinetics in a Baboon Model: IgG Subclass Dependency

Coetzee

Pieters²,

Wyk³

et al. 2000

Thromb Haemost

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show abstract

“…Although canine ITP models have been previously described, they have not been well characterized and the platelet‐depleting antibodies or heterologous serum employed in these models are no longer available (M. Hosono, Kinki University, personal communication, May 12, 2009) (Tocantins & Stewart, ; Joshi & Jain, ; Hosono et al , ). Thus, to our knowledge, our model represents the only available large animal ITP model.…”

Section: Discussionmentioning

confidence: 99%

A novel canine model of immune thrombocytopenia: has immune thrombocytopenia (ITP) gone to the dogs?

et al. 2014

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Summary Canine immune thrombocytopenia (ITP) is analogous to human ITP, with similar platelet counts and heterogeneity in bleeding phenotype among affected individuals. With a goal of ultimately investigating this bleeding heterogeneity, a canine model of antibody-mediated ITP was developed. Infusion of healthy dogs with 2F9, a murine IgG2a monoclonal antibody to the canine platelet glycoprotein GPIIb (a common target of autoantibodies in ITP) resulted in profound, dose-dependent thrombocytopenia. Model dogs developed variable bleeding phenotypes, e.g. petechiae and haematuria, despite similar degrees of thrombocytopenia. 2F9 infusion was not associated with systemic inflammation, consumptive coagulopathy, or impairment of platelet function. Unexpectedly however, evaluation of cytokine profiles led to the identification of platelets as a potential source of serum interleukin-8 (IL8) in dogs. This finding was confirmed in humans with ITP, suggesting that platelet IL8 may be a previously unrecognized modulator of platelet-neutrophil crosstalk. The utility of this model will allow future study of bleeding phenotypic heterogeneity including the role of neutrophils and endothelial cells in ITP.

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“…73,172–177 These include mouse models such as (NZW × BXSB) F1 mice 173 that develop lupus nephritis, myocardial infarction, and thrombocytopenia; and an immunodeficient SCID mouse/human chimera model, in which human cord blood cells or splenocytes from ITP patients were implanted into SCID mice. 174 Other animal models such as murine, 178,179 rat, 175 dog, 176 and baboon 177 have been studied, which were generated by injection of anti-β3 integrin antibodies. In models of alloimmune thrombocytopenia, genetically or chemically modified anti-HPA-1a competitive antibodies (B2G1 and SZ21) have been demonstrated to be able to block anti-HPA-1a antibodies binding to HPA-1a-positive platelets in murine models, suggesting their therapeutic potential.…”

Section: Animal Models Of Fnaitmentioning

confidence: 99%

Platelets and platelet alloantigens: Lessons from human patients and animal models of fetal and neonatal alloimmune thrombocytopenia

et al. 2015

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Platelets play critical roles in hemostasis and thrombosis. Emerging evidence indicates that they are versatile cells and also involved in many other physiological processes and disease states. Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a life threatening bleeding disorder caused by fetal platelet destruction by maternal alloantibodies developed during pregnancy. Gene polymorphisms cause platelet surface protein incompatibilities between mother and fetus, and ultimately lead to maternal alloimmunization. FNAIT is the most common cause of intracranial hemorrhage in full-term infants and can also lead to intrauterine growth retardation and miscarriage. Proper diagnosis, prevention and treatment of FNAIT is challenging due to insufficient knowledge of the disease and a lack of routine screening as well as its frequent occurrence in first pregnancies. Given the ethical difficulties in performing basic research on human fetuses and neonates, animal models are essential to improve our understanding of the pathogenesis and treatment of FNAIT. The aim of this review is to provide an overview on platelets, hemostasis and thrombocytopenia with a focus on the advancements made in FNAIT by utilizing animal models.

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Kinetics of platelets in dogs with thrombocytopenia induced by antiglycoprotein IIb/IIIa receptor monoclonal antibody

Cited by 8 publications

References 15 publications

The Effect of Monoclonal Anti-human-platelet Antibodies on Platelet Kinetics in a Baboon Model: IgG Subclass Dependency

The Effect of Monoclonal Anti-human-platelet Antibodies on Platelet Kinetics in a Baboon Model: IgG Subclass Dependency

A novel canine model of immune thrombocytopenia: has immune thrombocytopenia (ITP) gone to the dogs?

Platelets and platelet alloantigens: Lessons from human patients and animal models of fetal and neonatal alloimmune thrombocytopenia

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