Press Review
Press Review
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DOI：
10.1111/j.1423-0410.2010.01461.x
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发表时间：
2011-08
期刊：
影响因子：
2.7
通讯作者：
中科院分区：
文献类型：
--
作者：
在自身免疫性疾病中，自身反应性T细胞在抗原呈递细胞呈递自身抗原后被激活。对静脉注射免疫球蛋白（IVIg）治疗的自身免疫患者进行的几项临床研究以及几项体外研究表明，IVIg可以减少多克隆T细胞活化并改变其细胞因子分泌模式。然而，它们对（自身）抗原特异性T细胞应答的影响从未被直接解决。在本工作中，体内模型的诱导抗原特异性T细胞反应和体外抗原呈递系统被用来研究IVIg对T细胞反应的影响。所得结果表明，IVIg抑制体内和体外抗原特异性T细胞应答，但这种效应是抗原呈递细胞抗原呈递能力降低的间接结果。IVIg的抑制作用不依赖于FccRIIb，表明IVIg必须干扰抗原呈递细胞上表达的FccR的活化，以降低其呈递抗原的能力。因此，通过减少抗原呈递来抑制T细胞应答可能有助于IVIg在自身免疫性疾病中的众所周知的抗炎作用。
In autoimmune diseases, self-reactive T-cells become activated after presentation of autoantigens by antigenpresenting cells. Several clinical studies done with intravenous immunoglobulin (IVIg)-treated autoimmune patients as well as several in vitro studies have revealed that IVIg can reduce polyclonal T-cell activation and modify their cytokine secretion pattern. However, their effect on (auto)antigen-specific T-cell responses has never been addressed directly. In the present work, an in vivo model of induction of antigen-specific T-cell responses and an in vitro antigen presentation system was used to study the effects of IVIg on T-cell responses. The results obtained showed that IVIg inhibited both the in vivo and in vitro antigen-specific T-cell responses but that this effect was the indirect consequence of a reduction in the antigen presentation ability of antigen-presenting cells. The inhibitory effect of IVIg was FccRIIb-independent, suggesting that IVIg must interfere with the activation of FccRs expressed on antigen-presenting cells to reduce their ability to present antigens. Such inhibition of T-cell responses by reducing antigen presentation may therefore contribute to the well-known anti-inflammatory effects of IVIg in autoimmune diseases.