Micromethod for demonstrating increased platelet surface immunoglobulin G: Findings in acute, chronic, and human immunodeficiency virus‐1‐related immunologic thrombocytopenias

Sthoeger, Dalia; Nardi, Michael A.; Travis, Susan F.; Karpatkin, Margaret; Karpatkin, Simon

doi:10.1002/ajh.2830340408

Cited by 5 publications

(2 citation statements)

References 18 publications

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“…Flow cytometric evaluation of platelet-associated antibody has been used by several investigators of immunemediated thrombocytopenic purpura and HIV-1-associated thrombocytopenia (2,21,41,44). Alterations in mean platelet fluorescence and the appearance of distinct populations of platelets with different levels of platelet-associated Ig have been described previously (2).…”

Section: Discussionmentioning

confidence: 99%

Immune-mediated thrombocytopenia in horses infected with equine infectious anemia virus

Clabough

Gebhard

Flaherty

et al. 1991

J Virol

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An adult horse infected with a virulent, cell culture-adapted strain of equine infectious anemia virus (EIAV) developed cyclical thrombocytopenia in which the nadir of platelet counts coincided with peak febrile responses. In order to investigate the mechanism of thrombocytopenia during acute febrile episodes, four adult horses were experimentally infected with the wild-type Wyoming strain of EIAV. Platelet counts decreased from baseline as rectal temperature increased. Serum reverse transcriptase activity increased above background levels in all horses, coincident with increase in rectal temperature. All horses developed an EIAV-specific immune response detectable by Western immunoblot by postinfection day 10. Increases in platelet-associated immunoglobulins G and M were detectable by direct fluorescent-antibody test and flow cytometric assay. Viral replication in bone marrow megakaryocytes was not detectable by in situ hybridization. Results suggest an immune-mediated mechanism of thrombocytopenia in horses infected with EIAV. Despite an inability to identify virion particles in association with platelet-bound antibody, the cyclical nature of the thrombocytopenia and the occurrence of a marked cell-free viremia concomitant with fever and thrombocytopenia suggest immune complex deposition on platelets. We propose that clearance of virus and antibodycoated platelets from the peripheral circulation by hepatic Kupifer cells and splenic macrophages may target infectious virus particles, in the form of immune complexes, to host cells most permissive for in vivo viral replication. * Corresponding author. and for platelet-associated virus. We have also examined bone marrow for the presence of viral replication in megakaryocytes or megakaryocyte depletion.

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Section: Discussionmentioning

confidence: 99%

Immune-mediated thrombocytopenia in horses infected with equine infectious anemia virus

Clabough

Gebhard

Flaherty

et al. 1991

J Virol

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“…Acetylsalicylic acid was added to platelet-rich plasma followed by gel filtration of platelets as described (24). Lyophilized formalin-fixed platelets (Helena Laboratories, Beaumont, TX) were resuspended at 200,000/l in Tyrode's buffer prior to use.…”

Section: Platelet Preparationmentioning

confidence: 99%

Trophic Effects of Platelets on Cultured Endothelial Cells are Mediated by Platelet-associated Fibroblast Growth Factor-2 (FGF-2) and Vascular Endothelial Growth Factor (VEGF)

Pintucci

Froum²,

Pinnell³

et al. 2002

Thromb Haemost

111

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SummaryIn addition to their role in primary hemostasis, platelets serve to support and maintain the vascular endothelium. Platelets contain numerous growth factors including the potent angiogenic inducers VEGF and FGF-2. To characterize the function of these two plateletassociated growth factors, the effects of the addition of purified platelets to cultured endothelial cells were examined. The survival and proliferation of endothelial cells were markedly stimulated (2-3-fold and 5-15-fold respectively) by the addition of gel-filtered platelets. Acetylsalicylic acid-treated or lyophilized fixed-platelets were ineffective in supporting endothelial cell proliferation. In Transwell assays, the stimulatory effect of platelets on endothelial cells was preserved, consistent with an effect mediated by secreted factors. The combined inhibition of VEGF and FGF-2 by neutralizing antibodies, in contrast to inhibition of either alone, abrogated both platelet-induced endothelial cell survival and proliferation. FGF-2 isoforms were detected in platelet lysates, as well as in the releasates of agonist-stimulated platelets. Megakaryocytes generated by ex vivo expansion of hematopoietic progenitor cells with kit ligand and thrombopoietin were analyzed for expression of FGF-2. Punctate cytoplasmic staining but no nuclear staining was observed by immunocytochemistry consistent with possible localization of the growth factor to cytoplasmic granules. The addition of platelets to cultured endothelial cells activated extracellular signal-regulated kinase (ERK) in a dose and time-dependent manner. This effect was abrogated by both anti-FGF-2 and anti-VEGF antibody. Since FGF-2 and VEGF are potent angiogenic factors and known endothelial cell survival factors, their release by platelets provides a plausible mechanism for the platelet support of vascular endothelium.

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Analysis of platelets by flow cytometry in patients with Paroxysmal Nocturnal Hemoglobinuria (PNH)

Araten

Boxer

Zamechek

et al. 2020

Blood Cells, Molecules, and Diseases

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Micromethod for demonstrating increased platelet surface immunoglobulin G: Findings in acute, chronic, and human immunodeficiency virus‐1‐related immunologic thrombocytopenias

Cited by 5 publications

References 18 publications

Immune-mediated thrombocytopenia in horses infected with equine infectious anemia virus

Immune-mediated thrombocytopenia in horses infected with equine infectious anemia virus

Trophic Effects of Platelets on Cultured Endothelial Cells are Mediated by Platelet-associated Fibroblast Growth Factor-2 (FGF-2) and Vascular Endothelial Growth Factor (VEGF)

Analysis of platelets by flow cytometry in patients with Paroxysmal Nocturnal Hemoglobinuria (PNH)

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