Rocklin R E, Thistle L, Audera C
J Immunol. 1985 Sep;135(3):2033-9.
The effect of PGE2 and PGD2 on several lymphocyte functions in vitro was evaluated in nonatopic and atopic subjects. Both PGE2 and PGD2 inhibited phytohemagglutinin-induced protein synthesis ([3H] leucine uptake) by nonatopic mononuclear cells and T cells in a dose-dependent manner (10(-6) to 10(-12) M). Protein synthesis by atopic mononuclear cells was not significantly suppressed by the above concentration of PGE2. Although PGD2 effectively suppressed protein synthesis by atopic mononuclear cells and T cells at 10(-6) M, lower concentrations were ineffective. Kinetic studies revealed significant differences in the suppressive effects of PGE2 and PGD2 on atopic and nonatopic mononuclear cells at 24 and 48 h, but not at 72 or 96 hr. Protein synthesis by T helper-enriched populations (suppressor cell depletion by anti-Leu-2b + complement) obtained from nonatopics was significantly reduced by PGE2 and PGD2, suggesting that these mediators may be directly inhibiting the responding population. By contrast, protein synthesis by T suppressor-enriched populations (helper cell depletion by OKT4 + complement) obtained from nonatopics was enhanced by PGE2 and PGD2, suggesting that the PG were activating these cells. Atopic T helper and T suppressor cells exhibited decreased responsiveness to PGE2 and PGD2 compared with nonatopic cells. PGE2 and PGD2 inhibited the phytohemagglutinin-stimulated proliferative response ([3H]thymidine uptake) by both atopic and nonatopic mononuclear cells in a dose-dependent manner and to the same extent. However, although PGE2 and PGD2 generated functional suppressor activity (when using a coculture technique) in nonatopic mononuclear cells, these mediators failed to activate atopic suppressor cells. These results suggest that reduced responses by atopic T cells to signals provided by PGE2 and PGD2 are not solely restricted to suppressor cell function, and could indicate an impaired ability to regulate immune and/or inflammatory reactions.
在非特应性和特应性受试者中评估了前列腺素E2（PGE2）和前列腺素D2（PGD2）对几种淋巴细胞体外功能的影响。PGE2和PGD2均以剂量依赖性方式（10^(-6)至10^(-12)M）抑制非特应性单核细胞和T细胞中植物血凝素诱导的蛋白质合成（[3H]亮氨酸摄取）。上述浓度的PGE2对特应性单核细胞的蛋白质合成没有明显抑制作用。虽然PGD2在10^(-6)M时能有效抑制特应性单核细胞和T细胞的蛋白质合成，但较低浓度则无效。动力学研究表明，PGE2和PGD2在24小时和48小时对特应性和非特应性单核细胞的抑制作用存在显著差异，但在72小时或96小时时无差异。从非特应性个体获得的富含辅助性T细胞的群体（用抗Leu-2b加补体去除抑制细胞）的蛋白质合成被PGE2和PGD2显著降低，这表明这些介质可能直接抑制反应群体。相比之下，从非特应性个体获得的富含抑制性T细胞的群体（用OKT4加补体去除辅助细胞）的蛋白质合成被PGE2和PGD2增强，这表明前列腺素正在激活这些细胞。与非特应性细胞相比，特应性辅助性T细胞和抑制性T细胞对PGE2和PGD2的反应性降低。PGE2和PGD2以剂量依赖性方式且在相同程度上抑制特应性和非特应性单核细胞中植物血凝素刺激的增殖反应（[3H]胸腺嘧啶核苷摄取）。然而，虽然PGE2和PGD2在非特应性单核细胞中产生了功能性抑制活性（使用共培养技术时），但这些介质未能激活特应性抑制细胞。这些结果表明，特应性T细胞对PGE2和PGD2提供的信号反应降低不仅限于抑制细胞功能，还可能表明调节免疫和/或炎症反应的能力受损。
