Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals
Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals
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DOI：
10.1016/s1074-7613(00)80623-8
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发表时间：
1998-09-01
期刊：
影响因子：
32.4
通讯作者：
Longnecker, R
中科院分区：
文献类型：
--
作者：
Caldwell, RG;Wilson, JB;Longnecker, R
EB病毒(Epstein-Barr Virus，EBV)在人类外周B淋巴细胞中建立了一种持续的潜伏感染，与多种恶性肿瘤和增殖性疾病有关。潜伏膜蛋白2A(LMP2A)是体内仅有的两种在潜伏感染B淋巴细胞中表达的病毒蛋白之一。LMP2A通过结合Syk和Lyn蛋白酪氨酸激酶，在体外阻断B细胞受体(BCR)信号转导。为了分析LMP2A在体内表达的意义，建立了B细胞系表达LMP2A的转基因小鼠。LMP2A的表达导致绕过正常的B淋巴细胞发育检查点，允许免疫球蛋白阴性的细胞在外周淋巴器官定植，表明LMP2A在未转化的细胞中具有结构性信号活性。
Epstein-Barr virus (EBV) establishes a persistent latent infection in peripheral B lymphocytes in humans and is associated with a variety of malignancies and proliferative disorders. Latent membrane protein 2A (LMP2A) is one of only two viral proteins expressed in latently infected B lymphocytes in vivo. LMP2A blocks B cell receptor (BCR) signal transduction in vitro by binding the Syk and Lyn protein tyrosine kinases. To analyze the significance of LMP2A expression in vivo, transgenic mice with B cell lineage expression of LMP2A were generated. LMP2A expression results in the bypass of normal B lymphocyte developmental checkpoints allowing immunoglobulin-negative cells to colonize peripheral lymphoid organs, indicating that LMP2A possesses a constitutive signaling activity in nontransformed cells.