T-B-巨噬细胞构成了ITP发病机制的免疫细胞网络

T-B-Macrophage Axis forms the Immune Cell Network Underlying ITP Pathogenesis

摘要: 原发免疫性血小板减少症(ITP)的发病机制涉及多种免疫细胞的协同作用。B细胞异常活化产生抗血小板自身抗体、T细胞亚群失衡及直接细胞毒作用、巨噬细胞Fc受体介导的过度吞噬构成核心致病环节。具体而言，生发中心反应失控与长寿浆细胞的持续存活导致自身抗体不断产生；滤泡辅助性T细胞扩增伴随调节性T细胞功能缺陷，共同打破了机体的免疫耐受；而巨噬细胞向M1型极化及FcγR表达失衡则执行了血小板的清除过程。这三种细胞之间的相互作用是ITP发生发展的关键，也为解释临床治疗反应的差异性及开发联合靶向治疗策略提供了理论依据。

Abstract: The pathogenesis of primary immune thrombocytopenia (ITP) involves the coordinated interplay of multiple immune cells. Aberrant B cell activation leading to antiplatelet autoantibody production, T cell subset imbalance with direct cytotoxic effects, and Fc receptor-mediated excessive phagocytosis by macrophages constitute the core pathogenic mechanisms. Specifically, dysregulated germinal center reactions and sustained survival of long-lived plasma cells drive continuous autoantibody generation; expansion of follicular helper T cells coupled with defective regulatory T cell function collectively disrupts immune tolerance; while macrophage polarization toward the M1 phenotype and imbalanced FcγR expression execute platelet clearance. The interactions among these three cell types represent the critical determinant of ITP development and progression, providing a theoretical basis for explaining variability in clinical treatment responses and informing the development of combined targeted therapeutic strategies.