Journalartikel
Autorenliste: Bakchoul, Tamam; Sachs, Ulrich J.
Jahr der Veröffentlichung: 2016
Seiten: 187-194
Zeitschrift: Hämostaseologie
Bandnummer: 36
Heftnummer: 3
ISSN: 0720-9355
DOI Link: https://doi.org/10.5482/HAMO-14-09-0043
Verlag: Thieme Publishing
Abstract:
Immune thrombocytopenia (ITP) is an auto immune bleeding disorder characterized by isolated thrombocytopenia. A dysfunctional proliferation of autoreactive T cells is suggested to be responsible for the loss of tolerance to self-platelet antigens in ITP patients. Autoreactive T cells induce uncontrolled proliferation of autoantibody producing B cells leading to persistent anti-platelet autoimmunity in some ITP patients. The autoimmune response causes an increased destruction of platelets by antibody-mediated phagocytosis, complement activation but also by T cell mediated cytotoxicity. In addition, abnormalities in thrombopoiesis and insufficient platelet production due to antibody or T cell mediated megakaryocyte inhibition and destruction contribute to the pathophysiology of ITP. These various effector cell responses may account for the heterogeneity in the clinical manifestation of ITP and also, to success or failure of different treatment strategies. A better understanding of the mechanisms behind ITP will hopefully allow for better diagnostic and, particularly, therapeutic strategies in the future.
Zitierstile
Harvard-Zitierstil: Bakchoul, T. and Sachs, U. (2016) Platelet destruction in immune thrombocytopenia Understanding the mechanisms, Hämostaseologie, 36(3), pp. 187-194. https://doi.org/10.5482/HAMO-14-09-0043
APA-Zitierstil: Bakchoul, T., & Sachs, U. (2016). Platelet destruction in immune thrombocytopenia Understanding the mechanisms. Hämostaseologie. 36(3), 187-194. https://doi.org/10.5482/HAMO-14-09-0043
Schlagwörter
ANTIPLATELET ANTIBODIES; AUTOIMMUNE-DISEASES; BONE-MARROW; COMPLEMENT ACTIVATION; CONTROLLED-TRIAL; DOUBLE-BLIND; FC-GAMMA-RIIA; HELICOBACTER-PYLORI; MONOCLONAL-ANTIBODY; PLATELET