Measles virus inhibits mitogen-induced T cell proliferation but does not directly perturb the T cell activation process inside the cell.

Measles virus inhibits mitogen-induced T cell proliferation but does not directly perturb the T cell activation process inside the cell.
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麻疹病毒抑制丝裂原诱导的 T 细胞增殖,但不会直接干扰细胞内 T 细胞的激活过程。

DOI:
10.1016/0042-6822(92)90316-h
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发表时间:
1992
期刊:
影响因子:
3.7
通讯作者:
Oldstone,MB
Oldstone,MB
中科院分区:
医学3区
文献类型:
--
作者:
Yanagi,Y;Cubitt,BA;Oldstone,MB

文献摘要

被引文献

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麻疹病毒(MV)抑制患者的淋巴细胞功能,也抑制体外感染的细胞。在体外MV感染中,植物血凝素刺激的T淋巴细胞的增殖受到抑制,表现为与模拟感染细胞相比,[~3H]胸腺嘧啶核苷掺入细胞减少,细胞周期中S期的细胞频率降低。然而,MV感染本身并不完全阻止感染细胞中的DNA合成,因为通过荧光激活细胞分选器分离的在细胞表面表达MV抗原的感染T细胞仍然可以增殖。Northern印迹分析表明,在MV感染的细胞中,T细胞活化过程中诱导的IL-2、c-myc、IL-2受体、IL-6、c-myb和CDC-2等基因的表达没有受到明显抑制,表明MV不干扰T细胞的激活过程。当病毒感染24小时后加入抗MV血清或人工合成的抑制MV融合的寡肽苯甲氧基-D-Phe-L-Phe-Gly时,对T细胞增殖的抑制作用呈剂量依赖性逆转。根据这些结果,我们提出了MV抑制T细胞增殖的模型;感染细胞表面表达的MV糖蛋白与邻近T细胞细胞膜上的MV受体或其他分子相互作用,进而影响这些T细胞的增殖。
Measles virus (MV) inhibits lymphocyte function in patients, as well as in cells infectedin vitro. The proliferation of phytohemagglutinin-stimulated T lymphocytes is suppressed byin vitroMV infection, as shown by the diminished incorporation of [3H]thymidine into DNA and the reduced frequency of cells in the S phase of the cell cycle, as compared with mock-infected cells. MV infection itself, however, does not completely block DNA synthesis in infected cells, because infected T cells expressing MV antigens on the cell surface, isolated by fluorescence-activated cell sorter, could still proliferate. Northern blot analysis indicated that the expression of genes induced during T cell activation, such as those encoding interleukin 2 (IL-2), c-myc, IL-2 receptor, IL-6, c-myb, and cdc-2, was not significantly suppressed in MV-infected cells, suggesting that MV does not interfere with the T cell activation process. When anti-MV serum or carbobenzoxy-D-Phe-L-Phe-Gly, a synthetic oligopeptide known to inhibit MV-induced fusion, was added 24 hr after infection, the inhibition of T cell proliferation was reversed in a dose-dependent manner. From these results we propose a model for the inhibition of T cell proliferation by MV; MV glycoproteins expressed on the cell surface of infected cells interact with the MV receptor or other molecules on the cell membrane of adjacent T cells, which in turn affects the proliferation of those T cells.