Macrophages being the connecting link between innate and adaptive immune system plays a crucial role in microbial antigen presentation and orchestrates the subsequent clearance of microorganisms. Microbial invasion of macrophages trigger a plethora of signaling cascades, which interact among them to generate a dynamically altered hostile environment, that ultimately leads to disruption of microbial pathogenesis. Paradoxically, Mycobacterium sp. exploits macrophage proteins such as Coronin 1, Calcineurin, LRG47, SOCS1, CISH, Gbp5 etc. and secretes virulence proteins such as PknG, PtpA, SapM, Eis etc. to hijack these intra-macrophage, signaling cascades and thereby develop its own niche. Coronin 1, being a cortical protein is transiently recruited to all mycobacteria containing phagosomes, but only pathogenic mycobacteria can retain it on the phagosome, to hinder its maturation. Additionally, mycobacterial infection linked secretion of virulence factor Protein Kinase G through its phosphorylation, manipulates several macrophage signaling pathways and thus promotes pathogenesis at various stages, form early infection to latency to granuloma formation. Here we discuss the present status of mycobacteria engaged Coronin 1-dependent signaling cascades and secreted PknG related sequence of events promoting mycobacterial pathogenesis. Current knowledge about these two proteins in context of macrophage signaling manipulation encompassing diverse mechanisms like calcium-calcineurin signaling, reduced proinflamtory cytokine secretion, cytoskeletal changes, and adaptation in acidic environment, which ultimately converge toward mycobacterial survival inside the macrophages has been discussed.

巨噬细胞是先天免疫系统和适应性免疫系统之间的连接纽带，在微生物抗原呈递中起着至关重要的作用，并协调随后的微生物清除。巨噬细胞的微生物入侵触发了大量的信号级联，它们之间相互作用产生动态改变的恶劣环境，最终导致微生物发病机制的破坏。矛盾的是，分枝杆菌. 利用巨噬细胞蛋白如 Coronin 1、Calcineurin、LRG47、SOCS1、CISH、Gbp5 等，并分泌 PknG、PtpA、SapM、Eis 等毒力蛋白来劫持这些巨噬细胞内、信号级联，从而发展自己的生态位。Coronin 1 是一种皮质蛋白，它被瞬时招募到所有含有吞噬体的分枝杆菌中，但只有致病性分枝杆菌才能将其保留在吞噬体上，以阻碍其成熟。此外，分枝杆菌感染通过其磷酸化与毒力因子蛋白激酶 G 的分泌有关，操纵几种巨噬细胞信号通路，从而促进不同阶段的发病机制，从早期感染到肉芽肿形成的潜伏期。在这里，我们讨论分枝杆菌参与 Coronin 1 依赖性信号级联和分泌的 PknG 相关事件序列促进分枝杆菌发病机制的现状。目前关于这两种蛋白质在巨噬细胞信号传导操作背景下的知识包括多种机制，如钙-钙调神经磷酸酶信号传导、减少促炎细胞因子分泌、细胞骨架变化和酸性环境适应，最终收敛于巨噬细胞内的分枝杆菌存活。