Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Immunol Rev. 2011 Mar;240(1):235-51. doi: 10.1111/j.1600-065X.2010.00994.x.
Tuberculosis (TB) is a complex disease, and the success of the bacterium as an intracellular pathogen is the outcome of its close and longstanding coevolution with the mammalian host. The dialogue between Mycobacterium tuberculosis and the host is becoming understandable at the molecular, cellular, and tissue level. This has led to the elucidation of the (i) interaction between pattern recognition receptors and pathogen-associated molecular patterns, (ii) cross-talk between immune cells, and (iii) mechanisms underlying granuloma development. Disease as an eventual but not a necessary consequence of infection results from a sensitive balance between protective immunity and destructive pathology. Early events, governed largely by conserved mechanisms of host recognition, impact not only on type and course of adaptive immunity but also on lung parenchymal function. New interpretations of how these responses shape the lung environment and direct granuloma development emphasize that the disease results from pathologic consequences of non-resolving inflammation. We review recent advances in TB research within the context of this ambitious view of TB.
结核病（TB）是一种复杂的疾病，细菌作为细胞内病原体的成功是其与哺乳动物宿主密切而长期共同进化的结果。结核分枝杆菌与宿主之间的对话在分子、细胞和组织水平上逐渐变得清晰。这导致了（i）模式识别受体与病原体相关分子模式之间的相互作用，（ii）免疫细胞之间的串扰，以及（iii）肉芽肿发展的机制的阐明。疾病是感染的最终但不是必要的后果，是由于保护性免疫和破坏性病理之间的敏感平衡造成的。早期事件主要受宿主识别的保守机制控制，不仅影响适应性免疫的类型和过程，还影响肺实质功能。关于这些反应如何塑造肺部环境并指导肉芽肿发展的新解释强调，疾病是由非解决性炎症的病理后果引起的。我们在结核病的这一雄心勃勃的观点背景下，综述了结核病研究的最新进展。
