原发免疫性血小板减少症（ITP）是一种以抗体介导的血小板破坏为特点的自身免疫性疾病。B细胞功能异常在ITP发病中起到重要作用。CCR6为趋化因子受体，表达在成熟B细胞表面。CCR6与其配体CCL20共同参与了B细胞的免疫反应。我们前期研究发现ITP患者CCR6+B细胞比例、B细胞上CCR6表达水平和血浆中CCL20水平明显减低，且CCL20水平与抗血小板自身抗体相关。因次，我们推测异常表达CCR6/CCL20可能参与调控ITP中B细胞功能。在此基础上，我们进一步研究ITP患者CCR6+B细胞亚群及CCL20在ITP疾病中的临床意义，阐明CCR6+B细胞功能缺陷，并探索异常CCR6/CCL20对B细胞功能调控及趋化作用。另外，ITP小鼠体内实验干预CCR6/CCL20，观察其对ITP中B细胞的免疫异常是否具有逆转作用，为将来针对CCR6/CCL20的靶向治疗策略提供理论基础。

Primary immune thrombocytopenia (ITP) is an autoimmune disease characterized by antibody-mediated platelet destruction. The abnormal function of B cells plays a role in ITP. CCR6 expressed on mature B cells is a chemokine receptor. CCR6 and its ligand CCL20 are involved in the immune response of B cells. Our previous studies found that the frequency of CCR6+ B cells，the expression of CCR6 on B cells and the levels of CCL20 in plasma were significantly decreased in ITP patients. The levels of CCL20 were correlated with anti-platelet autoantibodies in ITP patients. Thus，we postulate that abnormal CCR6/CCL20 might participate in the dysfunction of B cells. On this basis, we will further study the clinical significance of CCL20 levels and CCR6+B subsets, clarify the dysfunction of CCR6+ B cells and explore the chemotactic and regulating effect of abnormal CCR6/CCL20 on B cells in ITP. Furthermore, we will intervene CCR6/CCL20 to observe whether the dysfunction of B cells could be reversed in ITP mouse models, which might provide a theoretical basis for targeted treatment strategies in future.