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传染性单核细胞增多症患者体内存在针对爱泼斯坦-巴尔病毒转化的B细胞系的细胞毒性效应细胞。

Cytotoxic effector cells specific for B Cell lines transformed by Epstein-Barr virus are present in patients with infectious mononucleosis.

作者信息

Svedmyr E, Jondal M

出版信息

Proc Natl Acad Sci U S A. 1975 Apr;72(4):1622-6. doi: 10.1073/pnas.72.4.1622.

Abstract

Peripheral lymphoid cells, from 12 cases of acute infectious mononucleosis (IM), were tested in a micro chromium-51 release assay for cytotoxic activity against a variety of cell lines that did or did not carry the Epstein-Barr virus (EBV) genome. Unfractionated lymphocytes from these patients were cytotoxic to both types of cell lines, as were lymphocytes from healthy individuals. If, however, lymphocytes bearing complement receptors were removed, the residual IM lymphocyte fraction was specifically cytotoxic for EBV-genome-carrying cell lines. The residual lymphocyte fraction in normal donors had no such effect. Heterophile-positive IM is caused by EBV, and these results indicate that, during the acute phase of this disease, patients harbor killer cells, probably T cells, which specifically kill EBV-genome-carrying B cells in vitro. No such specificity for EBV-genome-psitive target cells was found in normal lymphocytes stimulated in vitro with autologous EBV-genome-positive lymphoblastoid cells. Such stimulated cells were highly cytotoxic to both genome-positive and negative lines after removal of complement receptor-positive lymphocytes.

摘要

采用微量铬-51释放试验,检测了12例急性传染性单核细胞增多症(IM)患者外周血淋巴细胞对多种携带或不携带爱泼斯坦-巴尔病毒(EBV)基因组的细胞系的细胞毒活性。这些患者的未分离淋巴细胞对两种类型的细胞系均具有细胞毒性,健康个体的淋巴细胞也是如此。然而,如果去除带有补体受体的淋巴细胞,残留的IM淋巴细胞部分对携带EBV基因组的细胞系具有特异性细胞毒性。正常供体的残留淋巴细胞部分没有这种作用。嗜异性抗体阳性的IM由EBV引起,这些结果表明,在该疾病的急性期,患者体内存在杀伤细胞,可能是T细胞,它们在体外能特异性杀伤携带EBV基因组的B细胞。在用自体EBV基因组阳性淋巴母细胞体外刺激的正常淋巴细胞中,未发现对EBV基因组阳性靶细胞有这种特异性。去除补体受体阳性淋巴细胞后,这种刺激的细胞对基因组阳性和阴性细胞系均具有高度细胞毒性。

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本文引用的文献

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Transfer factor.转移因子
Adv Immunol. 1969;11:195-266. doi: 10.1016/s0065-2776(08)60480-0.
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T-lymphocyte proliferation in mononucleosis.单核细胞增多症中的T淋巴细胞增殖
Clin Immunol Immunopathol. 1973 Nov;2(1):114-20. doi: 10.1016/0090-1229(73)90041-x.

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