Sallinen K, Veräjänkorva E, Pöllänen P
Department of Obstetrics and Gynecology, University Central Hospital, Turku, Finland.
J Reprod Immunol. 2000 Mar;46(2):91-101. doi: 10.1016/s0165-0378(99)00061-3.
The molecular backgrounds of the anti-phospholipid syndrome and immunisation against the Rhesus proteolipid antigens are still largely unknown. In the present study, expression of (1) CD1, a major histocompatibility complex class l-like lipid antigen presenting molecule, (2) IL-10, a cytokine promoting induction of clonal anergy, and (3) CD80 and CD86, two T-cell costimulators preventing induction of clonal anergy when present, was investigated in frozen sections of cervix, corpus and the fallopian tube (FT) of 25-day-old BALB/c mice injected with FSH, progesterone or medium and of pregnant mice from each trimester (days 7, 14 and 19). CD1 was expressed by all endometrial epithelial cells. Enhanced immunostaining of the endometrial epithelial cells was observed after FSH treatment, and cervix and FT expressed generally more than the corpus of the uterus. After treatment with medroxy progesterone acetate (MPA), expression of CD1 by the endometrial epithelia was weak. During pregnancy CD1 was absent from the endometrium adjacent to the foetus, but was unaltered in the cervix and FT. IL-10 was expressed by the endometrial glands and also by the endometrial surface epithelium. MPA treatment increased the intensity of the IL-10 immunofluorescence. There were also chains of positive cells between the muscle bundles within the pregnant myometrium. CD80 and CD86 were usually absent from the female reproductive tract, but were occasionally found in the cervix during pregnancy. The present study demonstrates definite differences in the expression of both CD1 and IL-10 between the FSH and MPA treated mice, suggesting differences during the oestrous cycle. As IL-10 is expressed more in the secretory phase, it is probably involved in making the endometrium more acceptable for implantation by inducing clonal anergy. This is supported by the absence of CD80 and CD86. These results also suggest that abnormal expression of CD1d during pregnancy may predispose the mother for immunisation against lipid antigens such as membrane phospholipids and Rhesus-antigens.
抗磷脂综合征和针对恒河猴蛋白脂质抗原的免疫反应的分子背景在很大程度上仍然未知。在本研究中，对25日龄注射了促卵泡激素（FSH）、孕酮或培养基的BALB/c小鼠以及处于妊娠各期（第7、14和19天）的妊娠小鼠的子宫颈、子宫体和输卵管（FT）的冰冻切片，研究了以下几种物质的表达情况：（1）CD1，一种主要组织相容性复合体I类样脂质抗原呈递分子；（2）IL-10，一种促进克隆无能诱导的细胞因子；（3）CD80和CD86，两种共刺激分子，当存在时可防止克隆无能的诱导。所有子宫内膜上皮细胞均表达CD1。FSH处理后，观察到子宫内膜上皮细胞的免疫染色增强，子宫颈和输卵管的表达通常比子宫体更多。用醋酸甲羟孕酮（MPA）处理后，子宫内膜上皮细胞中CD1的表达较弱。在妊娠期间，与胎儿相邻的子宫内膜中不存在CD1，但在子宫颈和输卵管中未发生改变。IL-10由子宫内膜腺体以及子宫内膜表面上皮表达。MPA处理增加了IL-10免疫荧光的强度。在妊娠子宫肌层的肌束之间也有阳性细胞链。CD80和CD86通常在女性生殖道中不存在，但在妊娠期间偶尔在子宫颈中发现。本研究表明，FSH和MPA处理的小鼠之间CD1和IL-10的表达存在明显差异，提示在发情周期中存在差异。由于IL-10在分泌期表达更多，它可能通过诱导克隆无能使子宫内膜更易于接受着床。这得到了CD80和CD86缺失的支持。这些结果还表明，妊娠期间CD1d的异常表达可能使母亲易于针对脂质抗原如膜磷脂和恒河猴抗原产生免疫反应。
