Kumar R K
School of Pathology, University of New South Wales, Sydney, Australia.
Am J Pathol. 1989 Oct;135(4):605-14.
Immunogold-silver staining was used to identify T lymphocytes, T lymphocyte subsets, and B lymphocytes in lung tissue from mice injected intratracheally with silica, titanium dioxide, or saline alone. Morphometric quantitation revealed a marked influx of T lymphocytes in the silica-treated animals during the first 3 weeks after injection. The relative numerical density of these cells remained elevated when compared with saline-treated controls throughout the 12 weeks of the experiment. Cells expressing the CD4 and CD8 antigens were both increased in number, with the former accounting for approximately two-thirds of the T lymphocytes. An increased number of B lymphocytes was also apparent from 6 weeks after treatment with silica. The T lymphocyte response preceded the development of significant pulmonary fibrosis by several weeks. No lymphocyte response was observed in the lungs of mice injected with nonfibrogenic titanium dioxide. These observations are consistent with the hypothesis that lymphokines secreted by T lymphocytes play a role in the pathogenesis of silicotic inflammatory lesions and their progression to fibrosis.
采用免疫金银染色法鉴定经气管内注射二氧化硅、二氧化钛或仅注射生理盐水的小鼠肺组织中的T淋巴细胞、T淋巴细胞亚群和B淋巴细胞。形态计量学定量分析显示，在注射后的前3周，二氧化硅处理的动物中有大量T淋巴细胞流入。在整个12周的实验过程中，与生理盐水处理的对照组相比，这些细胞的相对数量密度一直保持升高。表达CD4和CD8抗原的细胞数量均增加，前者约占T淋巴细胞的三分之二。从二氧化硅处理6周后开始，B淋巴细胞数量也明显增加。T淋巴细胞反应比显著的肺纤维化发展提前数周。在注射非致纤维化二氧化钛的小鼠肺中未观察到淋巴细胞反应。这些观察结果与以下假设一致，即T淋巴细胞分泌的淋巴因子在矽肺炎症病变的发病机制及其向纤维化的进展中起作用。
