宿主识别结核菌（MTB）是由一系列不同定位的模式识别受体参与的动态过程。MTB可损伤吞噬体并释放相关分子到胞浆或甚至直接逃逸到胞浆中。然而，一旦进入胞内，其细胞壁中富含的糖组分如阿拉伯半乳聚糖（Arabinogalactan，AG）作为“非我”（non-self）组分如何被宿主识别至今未知。Galectin-8是一种重要的模式识别受体，其在MTB感染过程中的作用未见报道。我们前期发现，galectin-8可直接结合AG，且在MTB感染过程中，galectin-8可被“招募”至菌体，并促进NDP52与p62介导的选择性自噬，进而抑制MTB胞内存活。为此，本项目拟进一步研究galectin-8对AG的识别作用及该识别过程对MTB感染的调控机制。研究结果有望确立一种宿主细胞识别MTB感染的新模式，既能加深对MTB感染过程中基本生物学问题的理解，又能为结核病的药物治疗和疫苗设计提供新的分子靶标。

Macrophage is critical for host defense against Mycobacteriu tuberculosis (Mtb) infection. Though it has long been proposed that Mtb persists in the phagosome of macrophage by blocking phagosome maturation and fusion with lysosome, Mtb still releases different molecules including extracellular DNA and cyclic di-AMP from the phagosome or directly escapes from phagosome into the cytosol, followed by activation of cytosolic survellance pathway. Mtb cell wall is rich of glycans including arabinoglacan. However, it unknown how these non-self constituents escaped into the cytosol are sensed by host cells. Galectins are a type of animal lectin which specifically bind to beta-galactoside and serve as important pattern recognition receptors. Previously, we observed that 1) galectin-8 was recruited to Mtb in infected macrophage; 2) knockdown of galectin-8 significantly inhibited NDP52- and p62-mediated selective autophagy and enhanced intracellular survival of Mtb in macrophage; 3) galectin-8 directly interacted with arabinogalactan from larch wood; 4) arabinogalactan recruites galectin-8 and induces selective autophagy. Therefore, in this study we will further study whether galectin-8 is a receptor of cytosolic Mtb by recognition of arabinogalactan and calarify the downstream events and underlying mechanisms. Hopefully, we will identify a novel receptor in the recognition of cytosolic Mtb and provide a novel concept for cytosolic sensing of intracellular bacteria. This will further our understanding the fundamental biology of Mtb infection and provide novel molecule target for the development of drugs and vaccines against TB.