دورية أكاديمية
أعرض في EDS

Serum from half of patients with immune thrombocytopenia trigger macrophage phagocytosis of platelets.

التفاصيل البيبلوغرافية
العنوان: Serum from half of patients with immune thrombocytopenia trigger macrophage phagocytosis of platelets.
المؤلفون: Norris PAA; Innovation and Portfolio Management, Canadian Blood Services, Toronto, ON, Canada.; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.; Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada.; Toronto Platelet Immunobiology Group, Toronto, ON, Canada., Tawhidi Z; Innovation and Portfolio Management, Canadian Blood Services, Toronto, ON, Canada.; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.; Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada.; Toronto Platelet Immunobiology Group, Toronto, ON, Canada., Sachs UJ; Institute for Clinical Immunology, Transfusion Medicine, and Haemostasis, Justus Liebig University, Giessen, Germany.; Department of Thrombosis and Haemostasis, Giessen University Hospital, Giessen, Germany., Cserti-Gazdewich CM; Innovation and Portfolio Management, Canadian Blood Services, Toronto, ON, Canada.; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.; Laboratory Medicine Program, University Health Network, Toronto, ON, Canada.; University of Toronto Quality in Utilization, Education and Safety in Transfusion Research Program, University of Toronto, Toronto, ON, Canada., Lin Y; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.; University of Toronto Quality in Utilization, Education and Safety in Transfusion Research Program, University of Toronto, Toronto, ON, Canada.; Precision Diagnostics and Therapeutics Program, Sunnybrook Health Sciences Centre, Toronto, Canada., Callum J; Innovation and Portfolio Management, Canadian Blood Services, Toronto, ON, Canada.; University of Toronto Quality in Utilization, Education and Safety in Transfusion Research Program, University of Toronto, Toronto, ON, Canada.; Department of Pathology and Molecular Medicine, Kingston Health Sciences Centre and Queen's University, Kingston, ON, Canada., Gil Gonzalez L; Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada.; Toronto Platelet Immunobiology Group, Toronto, ON, Canada., Shan Y; Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada.; Toronto Platelet Immunobiology Group, Toronto, ON, Canada., Branch DR; Innovation and Portfolio Management, Canadian Blood Services, Toronto, ON, Canada.; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.; Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada.; University of Toronto Quality in Utilization, Education and Safety in Transfusion Research Program, University of Toronto, Toronto, ON, Canada.; Department of Medicine, University of Toronto, Toronto, ON, Canada.; Division of Hematology, Department of Medicine, University of Toronto, Toronto, ON, Canada., Lazarus AH; Innovation and Portfolio Management, Canadian Blood Services, Toronto, ON, Canada.; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.; Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Unity Health Toronto, Toronto, ON, Canada.; Toronto Platelet Immunobiology Group, Toronto, ON, Canada.; University of Toronto Quality in Utilization, Education and Safety in Transfusion Research Program, University of Toronto, Toronto, ON, Canada.; Department of Medicine, University of Toronto, Toronto, ON, Canada.
المصدر: Blood advances [Blood Adv] 2023 Jul 25; Vol. 7 (14), pp. 3561-3572.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Society of Hematology Country of Publication: United States NLM ID: 101698425 Publication Model: Print Cited Medium: Internet ISSN: 2473-9537 (Electronic) Linking ISSN: 24739529 NLM ISO Abbreviation: Blood Adv Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : American Society of Hematology, [2016]-
مواضيع طبية MeSH: Purpura, Thrombocytopenic, Idiopathic*/diagnosis , Thrombocytopenia*/metabolism, Humans ; Blood Platelets/metabolism ; Platelet Glycoprotein GPIIb-IIIa Complex/metabolism ; Immunoglobulin G ; Phagocytosis ; Macrophages/metabolism ; Autoantibodies
مستخلص: Humoral antiplatelet factors, such as autoantibodies, are thought to primarily clear platelets by triggering macrophage phagocytosis in immune thrombocytopenia (ITP). However, there are few studies characterizing the capacity and mechanisms of humoral factor-triggered macrophage phagocytosis of platelets using specimens from patients with ITP. Here, we assessed sera from a cohort of 24 patients with ITP for the capacity to trigger macrophage phagocytosis of normal donor platelets and characterized the contribution of humoral factors to phagocytosis. Sera that produced a phagocytosis magnitude greater than a normal human serum mean + 2 standard deviations were considered phagocytosis-positive. Overall, 42% (8/19) of MHC I alloantibody-negative ITP sera were phagocytosis-positive. The indirect monoclonal antibody immobilization of platelet antigens assay was used to detect immunoglobulin G (IgG) autoantibodies to glycoproteins (GP)IIb/IIIa, GPIb/IX, and GPIa/IIa. Autoantibody-positive sera triggered a higher mean magnitude of phagocytosis than autoantibody-negative sera. Phagocytosis correlated inversely with platelet counts among autoantibody-positive patients but not among autoantibody-negative patients. Select phagocytosis-positive sera were separated into IgG-purified and -depleted fractions via protein G and reassessed for phagocytosis. Phagocytosis was largely retained in the purified IgG fractions. In addition, we assessed serum concentrations of C-reactive protein, serum amyloid P, and pentraxin 3 as potential phagocytosis modulators. Pentraxin 3 concentrations correlated inversely with platelet counts among patients positive for autoantibodies. Taken together, sera from approximately half of the patients with ITP studied triggered macrophage phagocytosis of platelets beyond a normal level. An important role for antiplatelet autoantibodies in phagocytosis is supported; a role for pentraxins such as pentraxin 3 may be suggested.
(© 2023 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.)
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المشرفين على المادة: 0 (Platelet Glycoprotein GPIIb-IIIa Complex)
0 (Immunoglobulin G)
0 (Autoantibodies)
تواريخ الأحداث: Date Created: 20230412 Date Completed: 20230717 Latest Revision: 20240929
رمز التحديث: 20240929
مُعرف محوري في PubMed: PMC10368862
DOI: 10.1182/bloodadvances.2022009423
PMID: 37042934
قاعدة البيانات: MEDLINE
الوصف
تدمد:2473-9537
DOI:10.1182/bloodadvances.2022009423