Krenács T, Rosendaal M
Department of Anatomy and Developmental Biology, University College London, United Kingdom.
J Histochem Cytochem. 1995 Nov;43(11):1125-37. doi: 10.1177/43.11.7560895.
We investigated the expression of gap junction connexins26, -32, and -43 in normal, reactive, and diseased human lymphoid tissue with single and double immunolabeling and confocal laser scanning microscopy. In all tissues, connexin43 positivity was detected in follicular dendritic cells positive for CD21 and CD35 antigens, around lymphoendothelial cells moderately positive for Factor VIII, CD31 and cathepsin-D antigens; and somewhat in vascular endothelia including high endothelial venules strongly positive for Factor VIII and CD31 antigens. The ultrastructural hallmark of gap junctions, pentalaminar structures with appropriate spacing, was found in follicular dendritic cell processes. Connexin43 was also detected between smooth muscle and stromal cells of the gut, in capsular fibroblasts, and in tonsil epithelium. Neither connexin32 nor -26 was revealed, except for connexin26 in the tonsil epithelium. In follicular dendritic cells, connexin43 co-localized closely with the desmosomal proteins desmoplakin and desmoglein, suggesting that cell adherence has a role in gap junction formation. Most connexin43 was observed in sinus lining cells of lymph nodes involved in malignancies and in follicular dendritic cells in the light zone of germinal centers where maturing but still proliferating lymphocytes are situated. In the light of their distribution, gap junctions may play a part in regulating the growth of germinal centers and in integrating activating or controlling signals in follicular dendritic and sinus lining cell networks. Because connexin43 is the connexin of stromal cells, finding it in follicular dendritic cells in consistent with the proposal that these cells originate from resident stromal cells.
我们运用单标和双标免疫标记以及共聚焦激光扫描显微镜技术,研究了缝隙连接蛋白26、32和43在正常、反应性及患病人类淋巴组织中的表达情况。在所有组织中,缝隙连接蛋白43在CD21和CD35抗原呈阳性的滤泡树突状细胞中被检测到,在对VIII因子、CD31和组织蛋白酶D抗原呈中度阳性的淋巴内皮细胞周围;在包括对VIII因子和CD31抗原呈强阳性的高内皮微静脉在内的血管内皮中也有一定程度的表达。在滤泡树突状细胞突起中发现了缝隙连接的超微结构特征,即具有适当间距的五聚体结构。缝隙连接蛋白43在肠道平滑肌和基质细胞之间、被膜成纤维细胞以及扁桃体上皮中也被检测到。除了扁桃体上皮中的缝隙连接蛋白26外,未发现缝隙连接蛋白32和26。在滤泡树突状细胞中,缝隙连接蛋白43与桥粒蛋白桥粒斑蛋白和桥粒芯糖蛋白紧密共定位,提示细胞黏附在缝隙连接形成中起作用。在涉及恶性肿瘤的淋巴结窦内衬细胞以及生发中心亮区的滤泡树突状细胞中观察到了大部分缝隙连接蛋白43,生发中心亮区是成熟但仍在增殖的淋巴细胞所在之处。鉴于其分布情况,缝隙连接可能在调节生发中心的生长以及整合滤泡树突状细胞和窦内衬细胞网络中的激活或控制信号方面发挥作用。由于缝隙连接蛋白43是基质细胞的连接蛋白,在滤泡树突状细胞中发现它与这些细胞起源于驻留基质细胞的观点一致。