绝大多数肺结核是由结核分枝杆菌引发的，这种细菌通过阻断自然的免疫触发反应导致疾病的传染，而自然的免疫反应一旦发生，被感染的细胞就会死亡。新研究工作日前在线发表在《自然—免疫学》期刊上，为研制预防结核分枝杆菌疾病的新药开辟了一种可能的新途径。
结核分枝杆菌能感染一种名为巨噬细胞的免疫细胞，让它们成为临时性的细菌增生“孵化器”，增生的细菌被释放出来并去感染其他细胞。通常情况下，被感染的巨噬细胞会经历一种名为细胞凋亡的死亡过程并触发一种免疫反应。
Heinz Remold和同事发现，结构分枝菌阻止了巨噬细胞进入凋亡过程，但会通过一种名为“坏死”的方式让巨噬细胞死亡，这种细胞死亡的另一种方式让细菌得以逃脱宿主细胞并感染新细胞。
通过揭示结核分枝细胞逃离免疫系统的方式，新研究让人们更加深入地认识到结核病的发展过程。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Immunology，doi:10.1038/ni.1654，Huixian Gan，Heinz G Remold
Mycobacterium tuberculosis blocks crosslinking of annexin-1 and apoptotic envelope formation on infected macrophages to maintain virulence
Huixian Gan1, Jinhee Lee2, Fucheng Ren2, Minjian Chen1, Hardy Kornfeld2 & Heinz G Remold1
Abstract
Macrophages infected with attenuated Mycobacterium tuberculosis strain H37Ra become apoptotic, which limits bacterial replication and facilitates antigen presentation. Here we demonstrate that cells infected with H37Ra became apoptotic after the formation of an apoptotic envelope on their surface was complete. This process required exposure of phosphatidylserine on the cell surface, followed by deposition of the phospholipid-binding protein annexin-1 and then transglutaminase-mediated crosslinking of annexin-1 through its amino-terminal domain. In macrophages infected with the virulent strain H37Rv, in contrast, the amino-terminal domain of annexin-1 was removed by proteolysis, thus preventing completion of the apoptotic envelope, which resulted in macrophage death by necrosis. Virulent M. tuberculosis therefore avoids the host defense system by blocking formation of the apoptotic envelope, which leads to macrophage necrosis and dissemination of infection in the lung.
1 Brigham & Women's Hospital and Harvard Medical School, Boston, Massachusetts, 02115, USA.
2 Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
