Riccioli A, Filippini A, De Cesaris P, Barbacci E, Stefanini M, Starace G, Ziparo E
Institute of Histology and General Embryology, School of Medicine La Sapienza University, Rome, Italy.
Proc Natl Acad Sci U S A. 1995 Jun 20;92(13):5808-12. doi: 10.1073/pnas.92.13.5808.
The expression of the cell adhesion molecules ICAM-1, ICAM-2, and VCAM-1 and the secretion of the cytokine interleukin 6 have been measured in mouse Sertoli cells cultured in vitro. Cytometric analysis revealed that, in basal conditions, low levels of ICAM-1 and VCAM-1 were present on the surface of the cells, whereas treatment with interleukin 1, tumor necrosis factor alpha, lipopolysaccharide, or interferon gamma induced, with different kinetics, increases in their expression. ICAM-2 was not detectable in basal conditions, nor was it inducible. Electron microscopic analysis and binding experiments using 51Cr-labeled lymphocytes demonstrated that increased expression of ICAM-1 and VCAM-1 on the surface of Sertoli cells, induced by inflammatory mediators, determines an augmented adhesion between the two cell types. The same stimuli, with the exception of interferon gamma, produced a rapid and remarkable increment of interleukin 6 production by Sertoli cells. These results suggest the presence of both direct and paracrine mechanisms of interaction between Sertoli and immune-competent cells, possibly involved in the control of immune reactions in the testis. Such mechanisms are of interest for the understanding of autoimmune pathologies of the testis and, if confirmed in humans, they could be involved in the sexual transmission of human immunodeficiency virus infection.
在体外培养的小鼠支持细胞中,已对细胞黏附分子ICAM - 1、ICAM - 2和VCAM - 1的表达以及细胞因子白细胞介素6的分泌进行了检测。细胞计数分析显示,在基础条件下,细胞表面存在低水平的ICAM - 1和VCAM - 1,而用白细胞介素1、肿瘤坏死因子α、脂多糖或干扰素γ处理后,它们的表达会以不同的动力学增加。在基础条件下未检测到ICAM - 2,也无法诱导其表达。电子显微镜分析以及使用51Cr标记淋巴细胞的结合实验表明,炎症介质诱导支持细胞表面ICAM - 1和VCAM - 1表达增加,这决定了两种细胞类型之间黏附增强。除干扰素γ外,相同的刺激会使支持细胞产生白细胞介素6的量迅速且显著增加。这些结果表明支持细胞与免疫活性细胞之间存在直接和旁分泌相互作用机制,可能参与睾丸免疫反应的调控。这些机制对于理解睾丸自身免疫性疾病具有重要意义,如果在人类中得到证实,它们可能与人类免疫缺陷病毒感染的性传播有关。