The interleukin-10 homolog encoded by Epstein-Barr virus enhances the reactivation of virus-specific cytotoxic T cell and HLA-unrestricted killer cell responses.
The interleukin-10 homolog encoded by Epstein-Barr virus enhances the reactivation of virus-specific cytotoxic T cell and HLA-unrestricted killer cell responses.
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Epstein-Barr 病毒编码的白细胞介素 10 同源物可增强病毒特异性细胞毒性 T 细胞和 HLA 非限制性杀伤细胞反应的重新激活。
DOI：
10.1016/0042-6822(92)90253-l
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发表时间：
1992
期刊：
影响因子：
3.7
通讯作者：
Rooney,CM
中科院分区：
文献类型：
--
作者：
Stewart,JP;Rooney,CM
我们确定了EB病毒(EBV)编码的IL-10的同源物(病毒或VIL-10)对免疫反应的影响，这对控制EBV感染至关重要。我们在一株B细胞系中生产了重组VIL-10。重组蛋白的大小为17 kDa，与EB病毒感染的B细胞分泌的VIL-10分子量相同。通过抑制活化的白细胞产生干扰素-γ来显示重组VIL-10的功能活性。细胞毒性T细胞和人类白细胞抗原非限制性激活的杀伤细胞都是EBV免疫应答的重要武器。由B细胞刺激物表达或外源性添加的VIL-10可增强同种异体和EBV特异性细胞毒T细胞的体外再激活。VIL-10还能增强EBV转化的B细胞对人类白细胞抗原非限制性杀伤细胞的激活作用。相比之下，白介素2介导的这些杀手的激活没有受到影响。由于VIL-10在EBV的裂解周期中表达，我们认为在病毒体内复制期间，VIL-10的表达可能会增强对EBV感染细胞的免疫应答。通过这种方式，病毒可以限制自己的复制，并保持EBV特有的非致病原性病毒携带者状态。
We determined what influence the Epstein-Barr virus (EBV)-encoded homologue of IL-10 (viral or vIL-10) had on immune responses important for the control of EBV infection. We produced recombinant vIL-10 in a B cell line. A 17-kDa recombinant protein was secreted and had the same molecular weight as vIL-10 secreted by EBV-infected B cells. Functional activity of recombinant vIL-10 was shown by the inhibition of interferon-γ production by activated leukocytes. Cytotoxic T cells and HLA-unrestricted activated killer cells are both important arms of the immune response to EBV. vIL-10, either expressed by B cell stimulators or added exogenously, enhanced thein vitroreactivation of allo- and EBV-specific cytotoxic T cells. vIL-10 also enhanced the activation of HLA-unrestricted killer cells by EBV-transformed B cells. In contrast, the interleukin-2-mediated activation of these killers was unaffected. Since vIL-10 is expressed during the lytic cycle of EBV, we conclude that the expression of vIL-10 may enhance immune responses to EBV-infected cells during periods of virus replicationin vivo. In this way, the virus may limit its own replication and maintain the apathogenic virus carrier state that is characteristic of EBV.