Ehlers S
Molecular Infection Biology, Research Centre Borstel, D-23845 Borstel, Germany.
Ann Rheum Dis. 2003 Nov;62 Suppl 2(Suppl 2):ii37-42. doi: 10.1136/ard.62.suppl_2.ii37.
Studies in mouse infection models clearly demonstrate tumour necrosis factor (TNF) to be a critical component of both the antibacterially protective and the inflammatory immune response to Mycobacterium tuberculosis. It is therefore not surprising that treatment of patients-for example, those with rheumatoid arthritis-with biological agents interfering with TNF activity have shown an increased risk of reactivating tuberculosis. However, conceivably, TNF targeting biological agents can be developed that because of their particular mode of action and their specific pharmacodynamics may be less likely to have this side effect.
对小鼠感染模型的研究清楚地表明，肿瘤坏死因子（TNF）是抗结核分枝杆菌的保护性免疫反应和炎症免疫反应的关键组成部分。因此，使用干扰TNF活性的生物制剂治疗患者（例如类风湿性关节炎患者）会增加结核病复发风险也就不足为奇了。然而，可以想象，由于其特定的作用方式和特定的药效学，可能会开发出靶向TNF的生物制剂，其产生这种副作用的可能性较小。
