CD4+ T cells inhibit growth of Epstein-Barr virus-transformed B cells through CD95-CD95 ligand-mediated apoptosis.
CD4+ T cells inhibit growth of Epstein-Barr virus-transformed B cells through CD95-CD95 ligand-mediated apoptosis.
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DOI：
10.1093/intimm/10.8.1149
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发表时间：
1998-08
影响因子：
4.4
通讯作者：
A. D. Wilson;I. Redchenko;Neil A. Williams;A. Morgan
中科院分区：
文献类型：
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作者：
A. D. Wilson;I. Redchenko;Neil A. Williams;A. Morgan
超过90%的人群在婴儿期获得EB病毒（EBV），并保留终身潜伏感染而无任何临床后果。然而，EBV已被鉴定为传染性单核细胞增多症的致病因子，并且与免疫抑制患者中的几种肿瘤包括地方性伯基特淋巴瘤和B细胞淋巴瘤相关。感染EBV的B细胞在体外转化并作为淋巴母细胞系连续生长。EBV转化的B细胞在体内的生长受免疫系统控制。对EBV免疫的研究主要集中在对病毒潜伏抗原特异性的MHC I类限制性CD 8+细胞毒性T细胞。本文报道了在体外通过自体EBV感染的B细胞刺激外周血淋巴细胞，所述细胞已被诱导表达裂解周期抗原，产生主要为CD 4 + T细胞的应答。此外，EBV感染的B细胞的生长也可以由这些活化的CD 4 + T细胞通过CD 95-CD 95配体（CD 95 L）介导的凋亡来调节。CD 95-CD 95 L介导的凋亡是正常B细胞生长调节的重要机制。由于EBV转化的B细胞仍然对这种机制敏感，因此体内EBV的控制可能不仅通过病毒特异性CD 8+细胞毒性T细胞免疫，而且通过B细胞生长的免疫调节的正常机制。
Greater than 90% of the human population acquire Epstein-Barr virus (EBV) in infancy and retain a lifelong latent infection without any clinical consequences. Nevertheless EBV has been identified as the causal agent of infectious mononucleosis, and is associated with several tumours including endemic Burkitt's lymphoma and B cell lymphomas in immunosupressed patients. B cells infected with EBV are transformed in vitro and grow continuously as lymphoblastoid cell lines. The growth of EBV-transformed B cells in vivo is controlled by the immune system. Studies on immunity to EBV have mainly focused on MHC class I-restricted CD8+ cytotoxic T cells specific for viral latent antigens. Here it is reported that in vitro stimulation of peripheral blood lymphocytes by autologous EBV-infected B cells, which have been induced to express lytic cycle antigens, gives rise to a predominantly CD4+ T cell response. Furthermore, the growth of EBV-infected B cells can also be regulated by these activated CD4+ T cells through apoptosis mediated by CD95-CD95 ligand (CD95L). CD95-CD95L-mediated apoptosis is an important mechanism of normal B cell growth regulation. As EBV-transformed B cells remain susceptible to this mechanism, the control of EBV in vivo may be not only by virus-specific CD8+ cytotoxic T cell immunity but also by normal mechanisms of immune regulation of B cell growth.