Ehlers S
Abteilung Immunchemie und Biochemische Mikrobiologie, Forschungszentrum Borstel.
Internist (Berl). 2003 Nov;44(11):1363-73. doi: 10.1007/s00108-003-1036-z.
The histopathological hallmark of infections with Mycobacterium tuberculosis is the development of centrally necrotizing granulomatous lesions. Granulomas are focal accumulations of mononuclear cells in various states of differentiation, in which the local activation of mycobacteria-infected macrophages by specific T cells takes place. On the one hand, this assures efficient containment of mycobacterial growth and demarcation of the infectious focus. On the other hand this is associated with the displacement of and irreversible damage to functionally vital organ tissue (predominantly in the lungs). New insights, emerging from animal models of infection, into the dynamic mechanisms regulating the induction, maintenance and caseation of tuberculous granulomas explain why highly effective anti-inflammatory therapies, e. g. administration of anti-TNF monoclonal antibodies, may result in reactivation of tuberculosis.
结核分枝杆菌感染的组织病理学特征是形成中央坏死性肉芽肿病变。肉芽肿是处于不同分化状态的单核细胞的局灶性聚集，其中被分枝杆菌感染的巨噬细胞会被特异性T细胞局部激活。一方面，这确保了对分枝杆菌生长的有效控制以及感染灶的界定。另一方面，这与功能重要的器官组织（主要是肺部）的移位和不可逆损伤有关。从感染动物模型中获得的关于调节结核性肉芽肿诱导、维持和干酪样坏死动态机制的新见解，解释了为什么高效的抗炎疗法，例如给予抗TNF单克隆抗体，可能会导致结核病复发。
