Matsuzaki N, Saji F, Okada T, Sawai K, Kameda T, Tanizawa O
Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.
J Reprod Immunol. 1991 Feb;19(2):101-14. doi: 10.1016/0165-0378(91)90011-e.
The immunosuppressive activity of a JEG-3 choriocarcinoma-derived factor in human IL-2-dependent T cell responses has been studied, together with its effect on IL-2-independent T cell responses induced by 10 nM TPA. The factor completely suppressed the IL-2-independent proliferative responses of T cells but failed to suppress antigenic expression of activation-associated CD 25 molecules. Further studies examined the effect of the factor on LAK cell generation induced by rIL-2. Recombinant IL-2-induced LAK cell proliferation was observed on Day 4 and Day 5, but not on Day 3. As the factor suppressed the responses of LAK cell proliferation, we tested whether it blocked the generation of Day 3, Day 4 and Day 5 LAK cells. The addition of the factor failed to suppress the generation of Day 3 LAK cells, while it partially suppressed the lytic activity of Day 4 LAK cells and completely suppressed that of Day 5 LAK cells. The data suggest the presence of a heterogeneous pattern for LAK cell generation; one without proliferation, but the other requiring proliferation, to acquire killer activity. Taken together with the evidence that the factor failed to suppress NK activity, the choriocarcinoma-derived factor suppressed only the proliferative events of immunocompetent cells, but inhibited neither their activation nor the differentiation events. This immunosuppressive factor might be involved in the prevention of host-mediated rejection of choriocarcinoma cells or maternal rejection of the fetus.
研究了源自JEG - 3绒毛膜癌的一种因子在人白细胞介素-2(IL - 2)依赖的T细胞反应中的免疫抑制活性,以及它对由10 nM佛波酯(TPA)诱导的IL - 2非依赖的T细胞反应的影响。该因子完全抑制了T细胞的IL - 2非依赖的增殖反应,但未能抑制激活相关的CD 25分子的抗原表达。进一步的研究考察了该因子对重组IL - 2诱导的淋巴因子激活的杀伤细胞(LAK细胞)生成的影响。在第4天和第5天观察到重组IL - 2诱导的LAK细胞增殖,但在第3天未观察到。由于该因子抑制了LAK细胞增殖反应,我们测试了它是否阻断第3天、第4天和第5天LAK细胞的生成。添加该因子未能抑制第3天LAK细胞的生成,而它部分抑制了第4天LAK细胞的杀伤活性,并完全抑制了第5天LAK细胞的杀伤活性。数据表明LAK细胞生成存在异质性模式;一种不发生增殖,但另一种需要增殖以获得杀伤活性。结合该因子未能抑制自然杀伤细胞(NK)活性的证据,源自绒毛膜癌的因子仅抑制免疫活性细胞的增殖事件,但既不抑制它们的激活也不抑制分化事件。这种免疫抑制因子可能参与了预防宿主介导的绒毛膜癌细胞排斥或母体对胎儿的排斥。