Interleukin-18, interferon-gamma, IP-10, and Mig expression in Epstein-Barr virus-induced infectious mononucleosis and posttransplant lymphoproliferative disease.
Interleukin-18, interferon-gamma, IP-10, and Mig expression in Epstein-Barr virus-induced infectious mononucleosis and posttransplant lymphoproliferative disease.
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Interleukin-18、interferon-gamma、IP-10 和 Mig 在 Epstein-Barr 病毒诱导的传染性单核细胞增多症和移植后淋巴细胞增殖性疾病中的表达。
DOI：
10.1016/s0002-9440(10)65119-x
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Tosato,G
中科院分区：
文献类型：
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作者：
Setsuda,J;Teruya-Feldstein,J;Harris,NL;Ferry,JA;Sorbara,L;Gupta,G;Jaffe,ES;Tosato,G
T细胞免疫缺陷在移植后淋巴细胞增生性疾病（PTLD）的发病机制中发挥重要作用，允许eb病毒（EBV）感染的B淋巴细胞肆无忌惮地扩增。然而，T细胞功能以外的因素可能有助于PTLD的发病机制，因为即使在严重的T细胞免疫缺陷的情况下，PTLD也很少发生，而T细胞免疫缺陷的胸腺小鼠可以排斥ebv永生化细胞。在这里，我们报告，通过半定量RT-PCR分析，与诊断为急性ebv诱导的传染性单核细胞增多症的淋巴组织相比，PTLD组织表达的IL-18、干扰素-γ (IFN-γ)、Mig和RANTES水平显著降低。其他细胞因子和趋化因子的表达水平相似。免疫组化证实，与传染性单核细胞增多症组织相比，PTLD组织含有较少的IL-18和Mig蛋白。IL-18主要是单核细胞产物，促进IFN-γ的分泌，从而刺激Mig和RANTES的表达。IL-18和Mig在小鼠体内均表现出抑制血管生成的抗肿瘤活性。这些结果证明了IL-18、IFN-γ、Mig和RANTES在急性EBV诱导的传染性单核细胞增多症淋巴组织中的表达高于PTLD组织，并提出了这些介质参与EBV感染关键宿主反应的可能性。
T cell immunodeficiency plays an important role in the pathogenesis of posttransplant lymphoproliferative disease (PTLD) by permitting the unbridled expansion of Epstein-Barr virus (EBV)-infected B lymphocytes. However, factors other than T cell function may contribute to PTLD pathogenesis because PTLD infrequently develops even in the context of severe T cell immunodeficiency, and athymic mice that are T-cell-immunodeficient can reject EBV-immortalized cells. Here we report that PTLD tissues express significantly lower levels of IL-18, interferon-γ (IFN-γ), Mig, and RANTES compared to lymphoid tissues diagnosed with acute EBV-induced infectious mononucleosis, as assessed by semiquantitative RT-PCR analysis. Other cytokines and chemokines are expressed at similar levels. Immunohistochemistry confirmed that PTLD tissues contain less IL-18 and Mig protein than tissues with infectious mononucleosis. IL-18, primarily a monocyte product, promotes the secretion of IFN-γ, which stimulates Mig and RANTES expression. Both IL-18 and Mig display antitumor activity in mice involving inhibition of angiogenesis. These results document greater expression of IL-18, IFN-γ, Mig, and RANTES in lymphoid tissues with acute EBV-induced infectious mononucleosis compared to tissues with PTLD and raise the possibility that these mediators participate in critical host responses to EBV infection.