Hauser G J, Lidor A, Zakuth V, Rosenberg H, Bino T, David M P, Spirer Z
Pediatric Immunology Unit, Tel-Aviv Medical Center, Israel.
Cancer Detect Prev Suppl. 1987;1:39-42.
Pregnancy is a natural allograft and the mechanisms for its non-rejection are obscure. Depression of maternal cellular immunity was suggested as a possible explanation. Interleukin-2(IL-2) is a lymphokine release from OKT4+ lymphocyte. This factor has a crucial role in the proliferation and differentiation of T cell subsets, and controls functions associated with immune rejection mechanisms. We therefore examined the ability of lymphocytes from women in the 3 trimesters of pregnancy to produce IL-2 in culture. Mononuclear cells were cultured with PHA for 48 h. The IL-2-containing supernatant was added to and supported the proliferation of an IL-2 dependent T cell line. Proliferation of this line indicated the IL-2 content of the added supernatant. Using this assay, IL-2 production in all 3 trimesters of pregnancy was adequate and comparable to that of lymphocytes from non-pregnant women. These results suggest that the proposed defect in cellular immunity during pregnancy is not mediated by an inability of the lymphocytes to produce IL-2.
妊娠是一种自然的同种异体移植,其不被排斥的机制尚不清楚。有人提出母体细胞免疫抑制可能是一种解释。白细胞介素-2(IL-2)是由OKT4 +淋巴细胞释放的一种淋巴因子。该因子在T细胞亚群的增殖和分化中起关键作用,并控制与免疫排斥机制相关的功能。因此,我们检测了妊娠三期女性淋巴细胞在培养物中产生IL-2的能力。将单核细胞与PHA一起培养48小时。将含IL-2的上清液加入并支持IL-2依赖的T细胞系的增殖。该细胞系的增殖表明了所添加上清液中的IL-2含量。使用该测定法,妊娠三期的IL-2产生量充足,且与非妊娠女性淋巴细胞的IL-2产生量相当。这些结果表明,所提出的妊娠期细胞免疫缺陷并非由淋巴细胞产生IL-2的能力不足所介导。