Abstract：
The normal autophagy flux is beneficial for the rapid elimination of phagocytic pathogens by macrophages. However, Mycobacterium tuberculosis interferes with the autophagy flux of macrophages to weaken their immune function and evade immune surveillance. In this study, we found that miRNA-215-5p was downregulated in tuberculosis patients. A potential diagnostic model for tuberculosis was established by combining miRNA-215-5p with three others differentially expressed microRNAs (miRNA-145-5p, miRNA-486-5p and miRNA-628-3p). Furthermore, we discovered that the up-regulated miRNA-215-5p could inhibit the maturation of autophagy by preventing the fusion of autophagosomes with lysosomes in macrophages. The role of TB-specific miRNA-215-5p in inhibiting auto-lysosome formation provides evidence of its potential role in Host-directed therapy for tuberculosis.
摘要：
正常的自噬通量有益于巨噬细胞对吞噬病原体的疾速清除。然而,结核分枝杆菌干扰巨噬细胞的自噬通量，削弱其免疫功能，逃避免疫监视。在这项研究中,我们发现miRNA-215-5p在结核病患者中下调.通过将miRNA-215-5p与其他三种差异表达的microRNA（miRNA-145-5p，miRNA-486-5p和miRNA-628-3p)。此外，我们发现上调的miRNA-215-5p可以通过阻止巨噬细胞中自噬体与溶酶体的融合来抑制自噬的成熟.TB特异性miRNA-215-5p在抑制自身溶酶体形成中的作用提供了其在针对结核病的宿主治疗中的潜在作用的证据。
