Figure 4.

Strategies employed by MTB to evade host defenses and promote its survival

The immune system of the host plays a crucial role in controlling MTB infection. However, MTB has developed various mechanisms to subvert the host immune response and ensure its survival within host cells. This figure highlights the key strategies employed by MTB: 1) Inhibition of Host Cell Apoptosis: MTB possesses virulence-associated genes that hinder host cell apoptosis, preventing the elimination of infected cells and promoting its own survival. 2) Macrophage Activation and Immune Suppression: Infection with a virulent strain of MTB induces macrophage activation, resulting in the increased release of the cytokine IL-10. This promotes the release of TNFR2 and the inactivation of TNF-α, which impairs the inflammatory response. Additionally, chronic exposure to bacterial, viral, and parasitic antigens can lead to the upregulation of the immune checkpoint receptor PD-1 on activated T cells. This, in turn, activates Tregs and contributes to immune suppression, enabling MTB to evade host immune surveillance. By employing these strategies, MTB can evade host defenses, survive within host cells, and establish a persistent infection. Abbreviations: MHC, major histocompatibility complex class; RCC, Receptor-chain complex; TGF-β, Transforming growth factor β; TNF-α, Tumor necrosis factor alpha.