Mycobacterium tuberculosis ( M.tb ) is a bacterial pathogen that has evolved in humans, and its interactions with the host are complex and best studied in humans. Myriad immune pathways are involved in infection control, granuloma formation, and progression to tuberculosis (TB) disease. Inflammatory cells, such as macrophages, neutrophils, conventional and unconventional T cells, B cells, NK cells, and innate lymphoid cells, interact via cytokines, cell-cell communication, and eicosanoid signaling to contain or eliminate infection but can alternatively mediate pathological changes required for pathogen transmission. Clinical manifestations include pulmonary and extrapulmonary TB, as well as post-TB lung disease. Risk factors for TB progression, in turn, largely relate to immune status and, apart from traditional chemotherapy, interventions primarily target immune mechanisms, highlighting the critical role of immunopathology in TB. Maintaining a balance between effector mechanisms to achieve protective immunity and avoid detrimental inflammation is central to the immunopathogenesis of TB. Many research gaps remain and deserve prioritization to improve our understanding of human TB immunopathogenesis.

中文翻译：

---

人类结核病的免疫病理学


结核分枝杆菌 （ M.tb ） 是一种在人类中进化的细菌病原体，它与宿主的相互作用很复杂，最好在人类中进行研究。无数的免疫途径参与感染控制、肉芽肿形成和进展为结核病 （TB） 疾病。炎症细胞，如巨噬细胞、中性粒细胞、常规和非常规 T 细胞、B 细胞、NK 细胞和先天性淋巴细胞，通过细胞因子、细胞间通讯和类花生酸信号传导相互作用以遏制或消除感染，但也可以介导病原体传播所需的病理变化。临床表现包括肺结核和肺外结核，以及结核后肺病。反过来，结核病进展的危险因素主要与免疫状态有关，除了传统的化疗外，干预措施主要针对免疫机制，突出了免疫病理学在结核病中的关键作用。维持效应机制之间的平衡以实现保护性免疫和避免有害炎症是 TB 免疫发病机制的核心。许多研究空白仍然存在，值得优先考虑，以提高我们对人类结核病免疫发病机制的理解。