中文摘要：

目的观察肥大细胞和关节成纤维样滑膜细胞（FLS）共培养对FLS分泌白细胞介素（IL）石的影响及其作用机制。方法应用免疫组化染色法观察肥大细胞在关节滑膜中的分布。分离培养RA患者的FLS，加入肥大细胞系LAD-2共培养或用Transwell小室隔离共培养，观察上清中FLS分泌的细胞因子IL-6的变化。结果LAD-2几乎不产生IL-6，FLS组IL石的浓度为（3019±57）μg／L，而FLS与等量LAD-2细胞共培养的IL-6浓度为（7150±114）μg/L（P〈0．01）。且其增加程度与LAD-2细胞数量呈正相关。以4％甲醛固定和Transwell小室隔离两种方法分别阻断可溶性介质分泌和细胞间相互黏附，前一组中IL石增加可被阻断，但在后一组中不受影响。结论肥大细胞与FLS通过可溶性介质相互作用可增加FLS的IL石分泌，在RA发病中可能有重要意义。

英文摘要：

Objective To explore the significance of mast cells-fibroblast like synoviecytes （FLS） interaction in the pathogenesis of rheumatoid arthritis （RA）. Methods Frozen sections of RA synovia from 4 patients were made to observe the distribution of mast cells by immunechemistry. FLSs were isolated from 4 samples of RA synovia and co-cultured with the human mast cells of the line LAD-2 for 0, 12, 24, and 48 h, and 7 d. ELISA was used to detect the interleukin （IL）-6, an important proinflammatory cytokine. 4% formaldehyde was used to fix the FLS and LAD-2 cells and then detect the IL-6 levels in the supernatant. Other FLS and LAD-2 mast cells were put into the upper and lower chambers of Transwell system to be cocultured in isolate condition, an important proinflammatory cytokine. Results Microscopy showed that FLSs were adjacent to the mast cells. The IL-6 content of the FLS/LAD-2 cell co-culture supernatant was 7150 μg/L＋14 μg/L, significantly higher than that of the FLS supematant （3019 μg/L ＋57 μg/L, P 〈0. 01 ）. LAD-2 cell number dose-dependently increased the IL-6 content in the supernatant. Almost no IL-6 secretion was found in the supematant of the co-culture with fixed FLSs and non-fixe4d LAD-2 cells, and the IL-6 secretion in the supernatant of the cO-culture with fixed LAD-2 cells and non-fixed FLSs was similar to that of the single FLS group and far lower than that of the FLS-LAD-2 co-culture group. Transwell system test showed that there was no significant difference in the IL-5 level between the direct mixture co-culture group and indirect mixture co-culture. Conclusion Mast cell/FLS interaction increases the IL-6 secretion via soluble mediators, thus playing an important role in the pathogenesis of RA.