Lysis of tumor cells by CD3+4-8-16+ T cell receptor alpha beta- clones, regulated via CD3 and CD16 activation sites, recombinant interleukin 2, and interferon beta 1.

Lysis of tumor cells by CD3+4-8-16+ T cell receptor alpha beta- clones, regulated via CD3 and CD16 activation sites, recombinant interleukin 2, and interferon beta 1.
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CD3 4-8-16 T 细胞受体 αβ 克隆裂解肿瘤细胞,通过 CD3 和 CD16 激活位点、重组白细胞介素 2 和干扰素 β 1 进行调节。

DOI:
10.4049/jimmunol.138.5.1627
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发表时间:
1987
影响因子:
4.4
通讯作者:
R. Bolhuis
R. Bolhuis
中科院分区:
医学2区
文献类型:
--
作者:
R. J. Griend;W. Tax;B. A. V. Krimpen;R. Vreugdenhil;C. Ronteltap;R. Bolhuis

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一小部分正常的CD3+人T淋巴细胞(约2%)同时缺乏CD4和CD8抗原。我们已经从健康人和一名严重联合免疫缺陷患者的外周血淋巴细胞(PBL)中克隆了这些细胞。在7个CD3+4-8克隆中,有6个对各种所谓的NK敏感和不敏感的肿瘤靶细胞具有很强的杀伤活性。它们的靶细胞特异谱几乎可以和CD3-NK细胞来源的克隆一样宽,具有很强的裂解能力。其中一些克隆还具有抗体依赖性细胞毒性(ADCC),这是NK细胞来源克隆的特征,但不是CD3+4+或CD8+成熟T细胞来源克隆的特征。这种CD3+T细胞克隆不表达CD16(IgGFc受体)抗原,但正如我们在这里所展示的那样,CD16抗原可以在CD3+4-8-克隆上被识别出来。CD3+4-8-细胞的ADCC活性和CD16抗原表达均低于CD3-NK细胞克隆。CD3+4+或CD8+和CD3-NK细胞克隆的杀伤活性可分别被抗CD3或抗CD16的单抗增强,但CD3+4-8-克隆的杀伤活性可被这两种单抗增强。CD3+4+或CD8+克隆与重组IL 2共同孵育3小时后,CD3+4+或CD8+克隆的裂解活性显著增强,与CD3-NK细胞相同。提高同种异体特异性CD3+4+或CD8+克隆的裂解活性需要18小时的孵育。因此,CD3+4-8-16+细胞与CD3-NK细胞有几个共同的特征。然而,它们表达CD3抗原,这是CD4+或CD8+成熟T细胞的特征。我们的结果还表明,虽然CD3+4-8-克隆与五种被测试的抗CD3单抗发生反应,但这些克隆不表达典型的CD3+/Tiα,β抗原受体复合体。这一发现表明,CD3+4-8-克隆实际上不表达由WT31单抗鉴定的T细胞受体α、β链的共同表位。这些CD3+4-8-淋巴细胞可能代表具有特定免疫功能的不同T细胞亚群的成熟淋巴细胞。
A small subpopulation (about 2%) of normal CD3+ human T lymphocytes lacks both CD4 and CD8 antigens. We have cloned these cells from peripheral blood lymphocytes (PBL) obtained from healthy individuals and from a patient with severe combined immunodeficiency. Six out of seven CD3+4-8-clones exert strong cytolytic activity against a variety of so-called NK-susceptible and -nonsusceptible tumor target cells. Their target cell specificity spectrum can virtually be as wide as that of CD3-NK cell-derived clones, with strong lytic capacity. Some of these clones also exert antibody-dependent cellular cytotoxicity (ADCC), a characteristic of NK cell-derived clones but not of CD3+4+ or CD8+ mature T cell-derived clones. Such CD3+ T cell clones do not express the CD16 (IgG Fc receptor) antigen, but as we demonstrate here, the CD16 antigen can be identified on CD3+4-8-clones. Both ADCC activity and CD16 antigen expression are lower in CD3+4-8- than in CD3- NK cell clones. Lytic activity of mature CD3+4+ or CD8+ and CD3- NK cell clones can be augmented, respectively, by anti-CD3 or anti-CD16 monoclonal antibodies (MAb), but that of CD3+4-8- clones are augmented by both MAb. Lytic activity of CD3+4+ or CD8+ clones is considerably enhanced after 3 hr of incubation with recombinant IL 2, as found for CD3- NK cells. Enhancement of lytic activity of allospecific CD3+4+ or CD8+ clones requires 18 hr of incubation. Thus, CD3+4-8-16+ cells share several features with CD3- NK cells. However, they express the CD3 antigen, which is characteristic for CD4+ or CD8+ mature T cells. Our results also indicate that although CD3+4-8- clones react with five preparations of anti-CD3 MAb tested, these clones do not express a classical CD3+/Ti alpha, beta antigen receptor complex. This is suggested by the finding that the CD3+4-8- clones do virtually not express the common epitope of the T cell receptor alpha, beta-chains as identified by the WT31 MAb. These CD3+4-8- lymphocytes may represent functionally mature lymphocytes of a distinct T cell subpopulation having a particular immune function.