Schoenaker Jente M, Nelson Vivianne S, Henderickx Jannie G E, Terveer Elisabeth M, Jansen A J Gerard, Porcelijn Leendert, Netelenbos Tanja, Schipperus Martin R, Kapur Rick
Department of Experimental Immunohematology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, 1066 CX Amsterdam, the Netherlands.
Department of Experimental Immunohematology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, 1066 CX Amsterdam, the Netherlands; Department of Hematology, HagaZiekenhuis, 2545 AA The Hague, the Netherlands; Department of Hematology, Leiden University Medical Center, 2333 ZA Leiden, the Netherlands.
Blood Rev. 2025 Jan;69:101252. doi: 10.1016/j.blre.2024.101252. Epub 2024 Dec 9.
Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by enhanced platelet destruction and impaired platelet production, due to a loss of immune tolerance that leads to targeting of platelets and megakaryocytes by glycoprotein-autoantibodies and/or cytotoxic T cells. There is a high degree of heterogeneity in ITP patients signified by unpredictable disease trajectories and treatment responses. Initial studies in humans have identified intestinal microbiota perturbance in ITP. Recently, gut microbial perturbance has been linked to other autoimmune diseases. Based on these findings, we hypothesize that intestinal microbiota may influence ITP pathophysiology through several mechanisms, including induction of platelet-autoantibody production, increasing complement-dependent platelet cytotoxicity, disturbing T cell homeostasis, impairing megakaryocyte function, and increasing platelet-desialylation and -clearance. The pathophysiological heterogeneity of ITP may, at least in part, be attributed to a perturbed intestinal microbiota. Therefore, a better understanding of intestinal microbiota in ITP may result in a more personalized therapeutic approach.
免疫性血小板减少症（ITP）是一种自身免疫性出血性疾病，其特征是血小板破坏增强和血小板生成受损，这是由于免疫耐受丧失导致糖蛋白自身抗体和/或细胞毒性T细胞靶向血小板和巨核细胞所致。ITP患者存在高度异质性，表现为不可预测的疾病轨迹和治疗反应。对人类的初步研究已确定ITP患者存在肠道微生物群紊乱。最近，肠道微生物紊乱已与其他自身免疫性疾病相关联。基于这些发现，我们推测肠道微生物群可能通过多种机制影响ITP的病理生理学，包括诱导血小板自身抗体产生、增加补体依赖性血小板细胞毒性、扰乱T细胞稳态、损害巨核细胞功能以及增加血小板去唾液酸化和清除。ITP的病理生理异质性可能至少部分归因于肠道微生物群紊乱。因此，更好地了解ITP中的肠道微生物群可能会带来更个性化的治疗方法。
