Induction of apoptosis in Herpesvirus saimiri-immortalized T lymphocytes by blocking interaction of CD28 with CD80/CD86
Induction of apoptosis in Herpesvirus saimiri-immortalized T lymphocytes by blocking interaction of CD28 with CD80/CD86
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DOI：
10.1006/bbrc.1999.1364
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发表时间：
1999-09-24
影响因子：
3.1
通讯作者：
Adachi, A
中科院分区：
文献类型：
--
作者：
Akari, H;Fukumori, T;Adachi, A
我们先前已经证明了疱疹病毒能使原代猕猴T淋巴细胞永生化，在本研究中，我们检测了永生化T细胞的特征。细胞表型为CD3(+)、CD25(+)、CD69(+)、MHC-IIDR+，不产生感染性病毒，Hirt DNA中可检测到病毒DNA。有趣的是，主要的共刺激分子CD28及其配体CD80/CD86在永生化的T细胞上共表达。用抗CD28的中和性单抗处理细胞，阻断CD28与CD80/CD86的相互作用，导致细胞生长迟缓，并诱导细胞凋亡。抗体治疗的效果不能被外源性IL-2治疗所克服。这些发现表明CD28与CD80/CD86的相互作用对于人类免疫缺陷病毒永生化T细胞的最佳生长是必需的。(C)1999年学术出版社。
We have previously shown that Herpesvirus saimiri (HVS) immortalizes primary macaque monkey T lymphocytes, In this study, we examined the characteristics of the immortalized T cells. The cells showed the phenotype of activated T lymphoblasts (CD3(+) CD25(+) CD69(+) MHC-IIDR+) and produced no infectious virus while viral DNA was detected in the Hirt DNA. Interestingly, both a major costimulatory molecule, CD28, and its ligands, CD80/CD86, were coexpressed on the immortalized T cells. The treatment of the cells with a neutralizing monoclonal antibody against CD28, which blocks interaction of CD28 with CD80/CD86, resulted in retarded cell growth and in induction of apoptosis. The effect of the antibody treatment was not overcome by exogenous interleukin-2 treatment. These findings demonstrate the requirement of interaction of CD28 with CD80/CD86 for the optimal growth of HVS-immortalized T cells. (C) 1999 Academic Press.