免疫性血小板减少症（ITP）是一种常见的自身免疫性出血性疾病，骨髓是ITP患者血小板破坏的重要场所。以往关于ITP发病机制的研究多专注于免疫细胞对于造血细胞（巨核细胞和血小板）的杀伤和破坏。近年来，我们和国内外研究者均发现ITP患者骨髓造血组织自身也存在异常改变。异常的骨髓造血组织（如巨核细胞、嗜酸性粒细胞和造血基质细胞）有可能通过构成病理性微环境，影响具有骨髓区域特异性的长寿命浆细胞的存活及功能，参与ITP的发病并导致疾病迁延不愈。本项目中，我们拟通过研究ITP患者骨髓标本并构建两种主动型ITP小鼠模型，从体外和体内两方面探讨骨髓区域特异性的造血组织（如巨核细胞、嗜酸性粒细胞和造血基质细胞）调控骨髓长寿命浆细胞参与ITP发病的作用及机制，深入探索可能的免疫干预措施，为ITP尤其是难治性ITP的治疗提供新的思路。

Immune thrombocytopenia (ITP) is a common autoimmune disorder characterized with bleeding. Bone marrow is one of the main organs that contribute to platelet destruction. Previous studies on ITP pathogenesis mainly focused on the adaptive immunity by which the immune cells killed platelets and megakaryocytes. Nevertheless, the local hematopoietic tissues of bone marrow, including megakaryocytes, eosinophils, and hematopoietic stromal cells, displayed abnormality in patients with ITP according to recent studies. These regional cells may constitute a pathological microenvironment that contributes to the development and progress of ITP by several mechanism, e.g., in our hypothesis, by maintaining survival and function of the specialized long-lived plasma cells. Here, we will investigate this hypothesis by studies on bone marrow samples from both ITP patients and two types of ITP murine models. This study may shed lights on new mechanisms of ITP pathogenesis by which the regional tissue regulates long-lived plasma cells as well as on novel targets that can be used for clinical treatment of ITP.