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Blood:研究发现EB病毒如何逃避免疫系统的监测

来源:生物谷 2013-10-13 21:45

2013年10月14日讯 /生物谷BIOON/--近日,加拿大研究人员发现EB病毒感染如何逃避免疫系统的监测,新研究使得抗EB病毒(EBV)的疫苗发展向前迈进了一步。

EB病毒引起传染性单核细胞增多症和癌症如霍奇金淋巴瘤和鼻咽癌,霍奇金淋巴瘤和鼻咽癌是中国最常见的癌症。

仍然留存在体内的疱疹病毒家族成员感染喉咙中的上皮细胞和免疫B细胞。研究人员发现,病毒能触发关闭关键蛋白质的分子事件,使自然杀伤T细胞“看不见”受感染的细胞,自然杀伤T细胞是一类寻找和摧毁EB病毒感染细胞的免疫细胞。

Rusung Tan博士说:如果你能迫使关键蛋白质重新表达,那么你就可以使自然杀伤T细胞“看见”受感染的细胞,战胜病毒。这项研究结果发表在本周的科学Blood杂志上。(生物谷Bioon.com)

Innate immune control of EBV-infected B cells by invariant natural killer T cells

Brian K. Chung, et al.

Individuals with X-linked lymphoproliferative disease lack invariant natural killer T (iNKT) cells and are exquisitely susceptible to Epstein-Barr virus (EBV) infection. To determine whether iNKT cells recognize or regulate EBV, resting B cells were infected with EBV in the presence or absence of iNKT cells. The depletion of iNKT cells increased both viral titers and the frequency of EBV-infected B cells. However, EBV-infected B cells rapidly lost expression of the iNKT cell receptor ligand CD1d, abrogating iNKT cell recognition. To determine whether induced CD1d expression could restore iNKT recognition in EBV-infected cells, lymphoblastoid cell lines (LCL) were treated with AM580, a synthetic retinoic acid receptor-α agonist that upregulates CD1d expression via the nuclear protein, lymphoid enhancer-binding factor 1 (LEF-1). AM580 significantly reduced LEF-1 association at the CD1d promoter region, induced CD1d expression on LCL, and restored iNKT recognition of LCL. CD1d-expressing LCL elicited interferon γ secretion and cytotoxicity by iNKT cells even in the absence of exogenous antigen, suggesting an endogenous iNKT antigen is expressed during EBV infection. These data indicate that iNKT cells may be important for early, innate control of B cell infection by EBV and that downregulation of CD1d may allow EBV to circumvent iNKT cell-mediated immune recognition.

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