CLONAL ANALYSIS OF LYMPHOCYTES-T ISOLATED FROM OVARIAN-CARCINOMA ASCITIC FLUID - PHENOTYPIC AND FUNCTIONAL-CHARACTERIZATION OF T-CELL CLONES CAPABLE OF LYSING AUTOLOGOUS CARCINOMA-CELLS

CLONAL ANALYSIS OF LYMPHOCYTES-T ISOLATED FROM OVARIAN-CARCINOMA ASCITIC FLUID - PHENOTYPIC AND FUNCTIONAL-CHARACTERIZATION OF T-CELL CLONES CAPABLE OF LYSING AUTOLOGOUS CARCINOMA-CELLS
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DOI:
10.1002/ijc.1985.36.3.337
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发表时间:
1985-01-01
影响因子:
6.4
通讯作者:
MORETTA, L
MORETTA, L
中科院分区:
医学1区
文献类型:
--
作者:
FERRINI, S;BIASSONI, R;MORETTA, L

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从III-IV期卵巢癌患者腹水中分离的T淋巴细胞通过微培养系统克隆,该系统允许克隆几乎所有外周血人T淋巴细胞。在这些实验条件下,15%至42%的腹水T细胞产生克隆后代,分析其不同的功能能力。在获得的克隆中,36%-70%在PHA依赖性测定(使用P815作为靶细胞)中具有细胞溶解活性,该测定允许检测任何特异性的细胞溶解细胞。约一半的溶细胞克隆也裂解NK敏感的K562靶细胞。此外,30%-50%的总克隆在PHA刺激24小时后释放IL-2。在所有分析的患者中,可变比例(所有溶细胞克隆的11%-56%)对自体肿瘤细胞具有溶细胞活性。对其中一些克隆进行了更详细的分析:18/21表达T4-T8+表型,而其余3个为T4+ T8-。6个克隆中只有1个能裂解同种异体卵巢癌细胞,而5/8个克隆具有明确的NK样活性。8个克隆均被抗T11单克隆抗体抑制,7个克隆被抗T8单克隆抗体抑制。
T lymphocytes isolated from ascitic fluid of patients with stage III-IV ovarian carcinoma were cloned by means of a microculture system that allows cloning of virtually all peripheral blood human T lymphocytes. Under these experimental conditions, 15% to 42% of ascitic T cells gave rise to clonal progenies that were analyzed for different functional capabilities. Of the clones obtained, 36%-70% had cytolytic activity in a PHA-dependent assay (using P815 as target cells) that allowed detection of cytolytic cells of any specificity. About one-half of the cytolytic clones lysed the NK-sensitive K562 target cells as well. In addition, 30%-50% of the total clones released IL-2 upon stimulation with PHA for 24 hr. In all patients analyzed a variable proportion (11%-56% of all cytolytic clones) had cytolytic activity against autologous tumor cells. Some of these clones have been analyzed in more detail: 18/21 expressed the T4-T8+ phenotype, whereas the remaining 3 were T4+ T8-. Only one out of 6 clones tested lysed allogeneic ovarian carcinoma cells as well, while 5/8 had a definite NK-like activity. Finally, all 8 clones tested were inhibited by anti-T11 and 7/8 by anti-T8 monoclonal antibody.