Mycobacterium tuberculosis (M.tb) is likely the most successful human pathogen, capable of evading protective host immune responses and driving metabolic changes to support its own survival and growth. Ineffective innate and adaptive immune responses inhibit effective clearance of the bacteria from the human host, resulting in the progression to active TB disease. Many regulatory mechanisms exist to prevent immunopathology, however, chronic infections result in the overproduction of regulatory myeloid cells, like myeloid-derived suppressor cells (MDSC), which actively suppress protective host T lymphocyte responses among other immunosuppressive mechanisms. The mechanisms of M.tb internalization by MDSC and the involvement of host-derived lipid acquisition, have not been fully elucidated. Targeted research aimed at investigating MDSC impact on phagocytic control of M.tb, would be advantageous to our collective anti-TB arsenal. In this review we propose a mechanism by which M.tb may be internalized by MDSC and survive via the manipulation of host-derived lipid sources.

中文翻译：

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结核分枝杆菌和骨髓源性抑制细胞：深入了解富含小凹蛋白的脂筏。

结核分枝杆菌（M.tb）可能是最成功的人类病原体，能够逃避保护性宿主免疫反应并驱动代谢变化以支持其自身的生存和生长。无效的先天性和适应性免疫反应会抑制细菌从人类宿主中有效清除，从而导致活动性结核病的进展。存在许多调节机制来预防免疫病理学，然而，慢性感染会导致调节性骨髓细胞的过度产生，例如骨髓源性抑制细胞 (MDSC)，它在其他免疫抑制机制中积极抑制保护性宿主 T 淋巴细胞反应。MDSC 内化 M.tb 的机制以及宿主来源的脂质获取的参与尚未完全阐明。旨在调查 MDSC 对 M.tb 吞噬细胞控制影响的有针对性的研究将有利于我们的集体抗结核武器库。在这篇综述中，我们提出了一种机制，M.tb 可以通过 MDSC 内化并通过操纵宿主来源的脂质来源而存活。