Wojciak B, Crossan J F
Cell Biology Department, Glasgow University, UK.
Clin Exp Immunol. 1993 Jul;93(1):108-14. doi: 10.1111/j.1365-2249.1993.tb06505.x.
The accumulation of inflammatory cells in synovial tissue was studied using indirect immunofluorescence assays on cell cultures and frozen tissue sections of healing rat digital flexor tendons. Flexor tendons were collected from rats 3, 7 and 14 days after crush injury. Tendon sheath and epithenon cells were isolated by sequential enzymic digestion and cultured for 2 days. Subpopulations of synovial and inflammatory cells were identified with MoAbs against cell surface glycoproteins present on B lymphocytes (CD45), T lymphocytes (CD2, CD4, CD8), macrophages (CD14) and endothelial cells. A phagocytosis assay was also used to identify macrophages. We report a substantial increase in the number of T lymphocytes (mainly helper/inducer) and phagocytotic cells with monocyte/macrophage surface markers in tendon sheath and epitenon 3 days after crush injury. The infiltration of inflammatory cells into synovial sheath and epitenon preceded an increase in fibronectin production by tendon cells which was seen 7 days after injury. To study the interaction between T lymphocytes and synovial cells in vitro, we established synovial fibroblast-like type B cell cultures and used stimulated and non-stimulated T lymphocytes in cell binding assays. We observed increased adhesiveness between unstimulated synovial cells and synovial cells previously cultured with activated and non-activated T lymphocytes. ELISA inhibition studies have shown an increase in fibronectin production by synovial fibroblasts co-cultured with stimulated CD4+ T lymphocytes. We suggest that the presence of inflammatory cells in synovial sheath and epitenon during tendon healing induces synovial fibroblasts and epitenon cells to increase their production of fibronectin, which provides a scaffold for subsequent adhesion formation.
利用间接免疫荧光分析法，对愈合过程中的大鼠指屈肌腱的细胞培养物和冷冻组织切片进行研究，以观察滑膜组织中炎性细胞的聚集情况。在挤压伤后3天、7天和14天收集大鼠的屈肌腱。通过连续酶消化分离腱鞘和外皮细胞，并培养2天。用针对B淋巴细胞（CD45）、T淋巴细胞（CD2、CD4、CD8）、巨噬细胞（CD14）和内皮细胞表面存在的细胞表面糖蛋白的单克隆抗体来鉴定滑膜细胞和炎性细胞亚群。还采用吞噬试验来鉴定巨噬细胞。我们报告，挤压伤后3天，腱鞘和外皮中T淋巴细胞（主要是辅助/诱导性T淋巴细胞）以及具有单核细胞/巨噬细胞表面标志物的吞噬细胞数量大幅增加。炎性细胞浸润到滑膜鞘和外皮中，早于损伤后7天观察到的腱细胞纤连蛋白产生的增加。为了在体外研究T淋巴细胞与滑膜细胞之间的相互作用，我们建立了滑膜成纤维细胞样B细胞培养物，并在细胞结合试验中使用了经刺激和未经刺激的T淋巴细胞。我们观察到，未刺激的滑膜细胞与先前与活化和未活化T淋巴细胞共培养的滑膜细胞之间的黏附性增加。酶联免疫吸附测定抑制研究表明，与经刺激的CD4 + T淋巴细胞共培养的滑膜成纤维细胞产生的纤连蛋白增加。我们认为，肌腱愈合过程中滑膜鞘和外皮中炎性细胞的存在，诱导滑膜成纤维细胞和外皮细胞增加纤连蛋白的产生，这为随后的粘连形成提供了支架。
