Studies on immunosuppression indued by Measles Virus

用麻疹病毒（MV）感染外周血单个核细胞（PBMC）和T淋巴细胞，并与蛋白激酶C（PKC）激活剂佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）和钙离子载体离子霉素一起培养。刺激后，MV感染的细胞中的细胞活力和BrdU的掺入减少相比，模拟感染的细胞。DNA含量分析和末端脱氧转移酶（TdT）介导的dUTP缺口末端标记表明，MV感染，PMA加离子霉素激活的T淋巴细胞亚二倍体分数和DNA片段化增加。这些数据表明，MV诱导PMA加离子霉素激活的细胞中的凋亡性细胞死亡。与PMA加离子霉素的刺激相反，植物血凝素（PHA）的促有丝分裂刺激不会诱导MV感染细胞的凋亡细胞死亡，尽管细胞增殖受到抑制。诱导细胞凋亡。麻疹病毒（MV）感染的细胞可能是免疫抑制的机制之一，我们研究了麻疹病毒（MV）诱导的不同淋巴细胞群细胞内细胞因子水平的变化。MV感染和未感染的外周血单个核细胞与佛波醇2-肉豆蔻酸酯13-乙酸酯（PMA）加离子霉素在莫能菌素存在下培养10小时。表面抗原和细胞内细胞因子，白细胞介素（IL）-2，干扰素（IFN）-γ和IL-4，同时染色，并通过流式细胞术进行分析。MV感染的CD 3+、CD 4+、CD 8+淋巴细胞表达IL-2和IFN-γ的细胞百分比均显著高于未感染的淋巴细胞。IL-2主要在MV感染的CD 4+淋巴细胞中增加，而IFN-γ主要在MV感染的CD 8+淋巴细胞和γ δ T淋巴细胞中增加。IL-4的表达不受MV感染的影响。这些结果表明，MV提高了麻疹急性期细胞内1型细胞因子的水平。

Peripheral blood mononuclear cells (PBMC) and T lymphocytes were infected with measles virus (MV) and cultured with a protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate (PMA) and a calcium ionophore, ionomycin. After stimulation, cell viability and incorporation of BrdU were decreased in MV-infected cells compared to mock-infected cells. DNA content analysis and terminal deoxytransferase (TdT)-mediated dUTP nick end labeling demonstrated that the hypodiploid fraction and DNA fragmentation were increased in MV-infected, T lymphocytes activated with PMA plus ionomycin. These data suggest that MV induces apoptotic cell death in cells activated by PMA plus ionomycin. In contrast to stimulation with PMA plus ionomycin, mitogenic stimulation with phytohaemagglutinin (PHA) did not induce apoptotic cell death in MV-infected cells, although cell proliferation was suppressed. Apoptosis induced in stimulated. MV-infected cells may be one mechanism of immunosuppression.We investigated the changes in intracellular cytokine levels in different lymphocyte populations induced by measles virus (MV). MV-infected and uninfected peripheral blood mononuclear cells were cultured with phorbol 2-myristate 13-acetate (PMA) plus ionomycin in the presence of monensin for 10h. Surface antigen and intracellular cytokines, interleukin (IL)-2, interferon (IFN)-gamma, and IL-4, were stained simultaneously and analyzed by flow cytometry. The percentage of cells that expressed IL-2 and IFN-gamma was significantly increased in MV-infected CD3+, CD4+, CD8+ lymphocytes as compared with uninfected lymphocytes. IL-2 was increased mainly in MV-infected CD4+ lymphocytes, whereas IFN-gamma was increased mainly in MV-infected CD8+ lymphocytes and gammadelta T lymphocytes. Expression of IL-4 was unaffected by MV infection. These results demonstrate that MV enhances the intracellular levels of type 1 cytokines during the acute phase of measles.