The immunomodulatory effects of intravenous immunoglobulin therapy in Kawasaki disease.
The immunomodulatory effects of intravenous immunoglobulin therapy in Kawasaki disease.
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DOI：
10.1586/1744666x.2015.1044980
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发表时间：
2015
影响因子：
4.4
通讯作者：
Franco A
中科院分区：
文献类型：
--
作者：
Burns JC;Franco A
静脉注射免疫球蛋白（IVIG）用于调节急性川崎（KD）的炎症反应是一个巨大的治疗胜利。然而，三十年后，IVIG免疫调节的机制才刚刚开始被揭示。刺激分泌IL-10的树突状细胞（DC）的未成熟髓样细胞群和阐明Fc特异性、HLA限制性天然调节性T细胞（Treg）提供了对IVIG机制的深入了解。其他潜在机制包括提供药物特异性中和抗体、抗独特型和抗细胞因子抗体、阻断活化Fcγ受体和刺激抑制性FcγRIIb受体。新的倡议必须寻求了解IVIG的机制，以便有一天用更实惠和更有针对性的疗法取代它。
The introduction of intravenous immunoglobulin (IVIG) for modulation of inflammation in acute Kawasaki disease (KD) was a great therapeutic triumph. However, three decades later, the mechanisms underlying immune regulation by IVIG are only beginning to be revealed. Stimulation of an immature myeloid population of dendritic cells (DC) that secretes IL-10 and the elucidation of Fc-specific, HLA-restricted natural regulatory T cells (Treg) provide insights into mechanisms of IVIG. Other potential mechanisms include provision of agent-specific neutralizing antibody, anti-idiotype and anti-cytokine antibodies, blockade of activating Fcγ receptors, and stimulation of the inhibitory FcγRIIb receptor. New initiatives must seek to understand the mechanisms of IVIG in order to one day replace it with more affordable and more targeted therapies.