Department of Pathology, Medical School, University of Texas-Houston Medical School, Houston, Texas, USA.
Department of Pathology, Medical School, University of Texas-Houston Medical School, Houston, Texas, USA.
Tuberculosis (Edinb). 2013 Dec;93 Suppl:S3-9. doi: 10.1016/S1472-9792(13)70003-9.
Tuberculosis (TB) remains a significant public health burden worldwide. Treatment of this disease requires a minimum of six months and there is no vaccine available for the most common form of the disease. Increasing evidence suggests that the mycobacterial glycolipid trehalose 6,6' dimycolate (TDM; cord factor) plays a key role in the pathogenesis of TB disease. TDM protects the TB bacilli from macrophage-mediated killing, inhibits effective antigen presentation, and reduces the formation of protective T-cell responses. TDM promotes initiation of granuloma formation and likely plays a role in caseation. Furthermore, TDM may contribute to the development of post primary disease. Receptors for TDM were recently described and are expected to contribute to our knowledge of the molecular pathogenesis of TB disease. In this manner, understanding TDM may prove promising towards development of targeted TB therapeutics to limit clinical pathologies.
结核病（TB）仍然是全球重大的公共卫生负担。治疗这种疾病至少需要六个月的时间，而且对于最常见的疾病形式，尚无疫苗可用。越来越多的证据表明，分枝杆菌糖脂海藻糖 6,6'-二没食子酸酯（TDM；cord 因子）在结核病发病机制中起着关键作用。TDM 可保护结核杆菌免受巨噬细胞介导的杀伤，抑制有效的抗原呈递，并减少保护性 T 细胞反应的形成。TDM 促进肉芽肿形成的启动，并可能在干酪样坏死中起作用。此外，TDM 可能导致原发性疾病后发病。TDM 的受体最近被描述，并有望有助于我们了解结核病发病机制的分子发病机制。通过这种方式，了解 TDM 可能有助于开发针对结核病的靶向治疗药物，以限制临床病理。
