Deguchi Y, Kishimoto S
Third Department of Internal Medicine, Osaka University School of Medicine, Japan.
Clin Exp Immunol. 1991 Sep;85(3):392-5. doi: 10.1111/j.1365-2249.1991.tb05737.x.
The role of tumour necrosis factor-alpha (TNF-alpha) in the development of autoimmune pulmonary inflammation has been investigated in lupus-prone mice. An increase in TNF-alpha mRNA level from whole lung preparation of lupus-prone mice was evident, from 3 weeks to 12 weeks during growing process, as shown by Northern blot analysis, but not in control mice. Furthermore, it is also found that the major source of this increase in TNF-alpha mRNA was attributed to infiltrating mononuclear cells found within the lung. Treatment of lupus-prone mice with rabbit anti-mouse TNF-alpha IgG prevented the development of pulmonary inflammation lesions such as lung fibrosis and alveolitis. These results suggest that an increased TNF-alpha production by infiltrating mononuclear cells in the lungs of lupus-prone mice may play a role in the development of autoimmune pulmonary inflammation and in significant changes of cytokines and the immune responses in pulmonary inflammation lesions of lupus-prone mice.
在易患狼疮的小鼠中，已经对肿瘤坏死因子-α（TNF-α）在自身免疫性肺部炎症发展中的作用进行了研究。如Northern印迹分析所示，在生长过程中，从3周到12周，易患狼疮小鼠的全肺标本中TNF-α mRNA水平明显升高，但对照小鼠中则没有。此外，还发现TNF-α mRNA这种升高的主要来源归因于肺内浸润的单核细胞。用兔抗小鼠TNF-α IgG治疗易患狼疮的小鼠可预防肺部炎症病变如肺纤维化和肺泡炎的发展。这些结果表明，易患狼疮小鼠肺内浸润的单核细胞产生的TNF-α增加可能在自身免疫性肺部炎症的发展以及易患狼疮小鼠肺部炎症病变中细胞因子和免疫反应的显著变化中起作用。
