Expression of prolactin receptors in murine lymphoid cells in normal and autoimmune situations.
Expression of prolactin receptors in murine lymphoid cells in normal and autoimmune situations.
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正常和自身免疫情况下小鼠淋巴细胞中催乳素受体的表达。
DOI：
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发表时间：
1993
影响因子：
4.4
通讯作者：
Mireille Dardenne
中科院分区：
文献类型：
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作者：
M. Gagnerault;P. Touraine;Wilson Savino;Paul A. Kelly;Mireille Dardenne
我们通过使用针对 PRL-R 胞外域的几个表位的生物素化抗 PRL-R 单克隆抗体进行流式细胞荧光分析，并使用聚合酶链式反应扩增，分析了鼠淋巴样细胞上催乳素受体 (PRL-R) 的表达。我们证明 PRL-R 在正常大鼠和小鼠造血组织中普遍表达。在两个初级淋巴器官（即胸腺和骨髓）中，> 90% 的细胞被抗 PRL-R mAb 标记，但胸腺细胞上的 PRL-R 密度（通过荧光强度评估）低于骨髓细胞。在外周淋巴器官中，携带PRL-R的细胞比例较小，我们可以清楚地区分各种荧光强度的细胞亚群。通过使用淋巴细胞群的经典标记，我们注意到来自脾脏、淋巴结和血液的所有 B 细胞和巨噬细胞都强烈表达 PRL-R。关于 T 细胞群，在四个胸腺细胞亚群中检测到较大比例 (> 85%) 的 PRL-R+ 细胞，与外周标记的较小比例 (50% 至 65%) 的 T 细胞形成对比。在 CD4+ 和 CD8+ 外周淋巴细胞亚群中观察到类似的 PRL-R+ 细胞百分比。重要的是，T细胞有丝分裂原Con A对胸腺细胞和脾细胞的刺激促进了细胞膜上PRL-R分子密度的增强。由于高催乳素血症与一些自身免疫性疾病有关，我们还研究了 NZB 自身免疫小鼠中 PRL-R 的表达。与正常动物中观察到的模式相反，NZB 小鼠中携带 PRL-R 的 T 细胞的频率以及每个细胞的 PRL-R 密度随着年龄的增长而增加，这表明在自身免疫情况下可能会出现 PRL/PRL-R 相互作用的一些不平衡。总之，我们的数据为更好地理解生理和病理情况下免疫系统中 PRL 的作用模式提供了分子基础。
We have analyzed the expression of prolactin receptors (PRL-R) on murine lymphoid cells by using flow cytofluorometry analysis with biotinylated anti-PRL-R mAb raised against several epitopes of the extracellular domain of the PRL-R and by using polymerase chain reaction amplification. We demonstrated that PRL-R were universally expressed in normal rat and mouse hematopoietic tissues. In both primary lymphoid organs, namely, thymus and bone marrow, > 90% of cells were labeled by the anti-PRL-R mAb, but the density of PRL-R (assessed by fluorescence intensity) was lower on thymocytes than on bone marrow cells. In peripheral lymphoid organs there were smaller proportions of cells bearing PRL-R and we could clearly distinguish cell subsets of various fluorescence intensities. By using classical markers for lymphoid cell populations, we noted that all B cells and macrophages from spleen, lymph nodes, and blood strongly expressed the PRL-R. Regarding T cell populations, large proportions (> 85%) of PRL-R+ cells were detected in the four thymocyte subsets, thus contrasting with the smaller proportions (50 to 65%) of T cells labeled in the periphery. Similar percentages of PRL-R+ cells were observed in CD4+ and CD8+ peripheral lymphocyte subsets. Importantly, the stimulation of thymocytes and spleen cells with the T cell mitogen Con A promoted an enhancement of the density of PRL-R molecules on the cell membranes. Because hyperprolactinemia is associated with some autoimmune diseases, we also investigated PRL-R expression in the NZB autoimmune mouse. In contrast to the pattern observed in normal animals, the frequencies of PRL-R-bearing T cells as well as the density of PRL-R per cell increased with age in NZB mice, suggesting that some imbalances of PRL/PRL-R interaction might occur in autoimmune situations. In conclusion, our data provide a molecular basis for a better understanding on the mode of action of PRL within the immune system in physiologic and pathologic situations.