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Lectin-dependent cell-mediated cytotoxicity and blastogenesis by large granular-enriched and depleted lymphocytes.

机译:凝集素依赖性细胞介导的细胞毒性和成骨作用由大量富含颗粒和耗尽的淋巴细胞组成。

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摘要

The role of larger granular-enriched and depleted lymphocytes was studied in lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 human epipharynx carcinoma target cells. LDCC was evaluated by detachment from the monolayer of 3H-thymidine-prelabelled HEp-2 cells in a 24 h assay at effector-target cell ratios of 25:1 and 50:1 in the presence of 25 micrograms/ml concanavalin A (Con A). Under the aforementioned conditions but in the absence of Con A natural cell-mediated cytotoxicity (NCMC) was not found. However, cytotoxicity was significantly augmented in the presence of Con A (= LDCC) using human peripheral blood mononuclear cells (PBMC) as effectors. Large granular lymphocytes (LGL), which show high natural killer (NK) activity to K 562 target cells, failed to be cytotoxic against HEp-2 targets similar to large granular depleted lymphocytes (LGL-DL). On the other hand, LGL caused only a slight LDCC; whilst LGL-DL induced strong LDCC activity towards HEp-2 targets. In comparison to LDCC using LGL-DL as effector cells, LGL and LGL-DL mixed at a ratio of 1:2, and added to target cells, had no major effect on LDCC, while a lower level of LDCC was observed at LGL/LGL-DL ratios of 1:1, and 2:1, suggesting the dilution of LGL-DL, potential effectors of LDCC to HEp-2 cells, rather than a specific regulatory role of LGL in LDCC. In parallel studies, the proliferation of LGL-DL in response to Con A was less than that observed with PBMC or LGL. The response could be restored by replacing half of LGL-DL per culture with an equal number of LGL, or by the addition of 10% monocytes. Significant functional differences between LGL and LGL-DL in LDCC as well as in Con A-induced blastogenesis are suggested.
机译:在凝集素依赖性细胞介导的细胞毒性(LDCC)对粘附的HEp-2人咽咽癌靶细胞的研究中,研究了较大颗粒的富集和耗尽的淋巴细胞的作用。 LDCC通过在25微克/毫升伴刀豆球蛋白A(Con A)存在的条件下,以25:1和50:1的效应子-靶细胞比率在24小时的测定中从3H-胸苷预标记的HEp-2细胞单层分离来评估)。在上述条件下,但在没有Con A的情况下,未发现天然细胞介导的细胞毒性(NCMC)。但是,使用人外周血单核细胞(PBMC)作为效应子,在Con A(= LDCC)存在下,细胞毒性显着增强。对K 562靶细胞表现出高自然杀伤(NK)活性的大颗粒淋巴细胞(LGL)不能像大颗粒耗尽淋巴细胞(LGL-DL)一样对HEp-2靶标产生细胞毒性。另一方面,LGL仅造成了轻微的LDCC;而LGL-DL诱导了针对HEp-2目标的强LDCC活性。与使用LGL-DL作为效应细胞的LDCC相比,LGL和LGL-DL以1:2的比例混合并添加到靶细胞中,对LDCC没有重大影响,而在LGL / LGL-DL比率为1:1和2:1,表明LGL-DL的稀释是LDCC对HEp-2细胞的潜在效应子,而不是LGL在LDCC中的特定调节作用。在平行研究中,响应Con A的LGL-DL的增殖少于PBMC或LGL的增殖。可以通过用等量的LGL替换每种培养物中一半的LGL-DL或添加10%单核细胞来恢复反应。提示LGL和LGL-DL在LDCC中以及在Con A诱导的胚发生中有重要的功能差异。

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