Intravenous immunoglobulin (IVIg) has been used for more than 25 years to treat an ever-increasing number of autoimmune diseases including immune thrombocytopenic purpura. Although the exact mechanism of action of IVIg has remained elusive, many theories have been postulated, including mononuclear phagocytic system blockade/inhibition, autoantibody neutralization by anti-idiotype antibodies, pathogenic autoantibody clearance due to competitive inhibition of the neonatal immunoglobulin Fc receptor, cytokine modulation, complement neutralization, and immune complex formation leading to dendritic cell priming. Polyclonal anti-D immunoglobulin is a polyclonal IVIg product enriched for antibodies directed to the RhD antigen on red blood cells and that has also been successfully used to treat immune thrombocytopenia in RhD(+) patients. The primary theory to explain polyclonal anti-D immunoglobulin function has classically been mononuclear phagocytic system blockade, although modulation of Fcgamma receptor expression and/or immunomodulation may also play a role. Work using a murine model of immune thrombocytopenic purpura to further our understanding of the mechanism of action of these 2 therapeutic agents is a focus of this article.

中文翻译：

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静脉免疫球蛋白和多克隆抗d免疫球蛋白在改善免疫性血小板减少性紫癜中的作用机制：我们真正知道什么？

静脉免疫球蛋白（IVIg）已用于治疗越来越多的自身免疫疾病，包括免疫性血小板减少性紫癜，已有25年以上的历史。尽管IVIg的确切作用机理仍然难以捉摸，但已经提出了许多理论，包括单核吞噬系统阻滞/抑制，抗独特型抗体对自身抗体的中和作用，由于竞争性抑制新生儿免疫球蛋白Fc受体引起的致病性自身抗体清除，细胞因子调节，补体中和和免疫复合物形成导致树突状细胞引发。多克隆抗D免疫球蛋白是富含针对红细胞上RhD抗原的抗体的多克隆IVIg产品，也已成功用于治疗RhD（+）患者的免疫性血小板减少症。解释多克隆抗D免疫球蛋白功能的主要理论传统上是单核吞噬系统阻滞，尽管Fcγ受体表达的调节和/或免疫调节也可能起作用。使用免疫性血小板减少性紫癜的小鼠模型来进一步了解这两种治疗剂的作用机理的工作是本文的重点。