Zheng Y, Zhou Z Z, Lyttle C R, Teuscher C
Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia 19104-6080.
J Leukoc Biol. 1988 Jul;44(1):27-32. doi: 10.1002/jlb.44.1.27.
Previous studies have shown that the injection of estrogen into immature rats leads to an influx of leukocytes into the uterus. Using immunoperoxidase staining and monoclonal antibodies, we have characterized the nature of the infiltrating leukocytes in frozen sections of immature rat uteri obtained following the injection of estrogen, estrogen plus pertussigen, and the antiestrogen LY117018. Estradiol treatment for 2 days resulted in a significant increase in the number of uterine eosinophils, CD4 (W3/W25)-positive helper/inducer T lymphocytes, macrophages (MRC OX-42-positive cells), and Ia (MRC OX-6)-positive cells. In contrast, estradiol treatment failed to elicit a significant increase in the number of CD8 (MRC OX-8)-positive uterine cytotoxic/suppressor T lymphocytes and/or natural killer cells, as well as MAR 18.5- and/or MRC OX-12-positive B lymphocytes. The injection of LY117018 failed to elicit any changes in the number of cells expressing any of the phenotypes under investigation. The simultaneous injection of pertussigen, the major toxin responsible for the leukocytosis- and lymphocytosis-promoting activity of Bordetella pertussis, inhibited the estrogen-induced influx of eosinophils, macrophages (MRC OX-42-positive cells), and Ia (MRC OX-6)-positive cells but failed to prevent the influx of CD4 (W3/25) positive helper/inducer T lymphocytes. These results indicate that, in the immature rat, significant differences may exist in the susceptibility of various cell populations to the effects of estrogen, particularly with regard to uterine influx following estrogen stimulation. In addition, our observations suggest that either 1) the CD4-positive cells infiltrating the uterus following estrogen treatment may use a nonpertussigen-sensitive mechanism for chemotactic factor-receptor signal transduction or 2) a subpopulation of resident uterine cells can be induced to express the CD4 antigen following estrogen and/or estrogen plus pertussigen treatment.
先前的研究表明,向未成熟大鼠注射雌激素会导致白细胞流入子宫。我们使用免疫过氧化物酶染色和单克隆抗体,对注射雌激素、雌激素加百日咳杆菌毒素以及抗雌激素LY117018后获得的未成熟大鼠子宫冰冻切片中浸润白细胞的性质进行了表征。用雌二醇处理2天导致子宫嗜酸性粒细胞、CD4(W3/W25)阳性辅助/诱导性T淋巴细胞、巨噬细胞(MRC OX - 42阳性细胞)和Ia(MRC OX - 6)阳性细胞的数量显著增加。相比之下,雌二醇处理未能使CD8(MRC OX - 8)阳性子宫细胞毒性/抑制性T淋巴细胞和/或自然杀伤细胞以及MAR 18.5和/或MRC OX - 12阳性B淋巴细胞的数量显著增加。注射LY117018未能引起所研究的任何表型细胞数量的变化。同时注射百日咳杆菌毒素(负责百日咳杆菌促白细胞增多和淋巴细胞增多活性的主要毒素)可抑制雌激素诱导的嗜酸性粒细胞、巨噬细胞(MRC OX - 42阳性细胞)和Ia(MRC OX - 6)阳性细胞的流入,但未能阻止CD4(W3/25)阳性辅助/诱导性T淋巴细胞的流入。这些结果表明,在未成熟大鼠中,各种细胞群体对雌激素作用的敏感性可能存在显著差异,特别是在雌激素刺激后的子宫细胞流入方面。此外,我们的观察结果表明,要么1)雌激素处理后浸润子宫的CD4阳性细胞可能使用对百日咳杆菌毒素不敏感的机制进行趋化因子 - 受体信号转导,要么2)驻留子宫细胞的一个亚群在雌激素和/或雌激素加百日咳杆菌毒素处理后可被诱导表达CD4抗原。