The Immune Escape Mechanisms of Mycobacterium Tuberculosis

Abstract

Epidemiological data from the Center of Disease Control (CDC) and the World Health Organization (WHO) statistics in 2017 show that 10.0 million people around the world became sick with tuberculosis. Mycobacterium tuberculosis (MTB) is an intracellular parasite that mainly attacks macrophages and inhibits their apoptosis. It can become a long-term infection in humans, causing a series of pathological changes and clinical manifestations. In this review, we summarize innate immunity including the inhibition of antioxidants, the maturation and acidification of phagolysosomes and especially the apoptosis and autophagy of macrophages. Besides, we also elaborate on the adaptive immune response and the formation of granulomas. A thorough understanding of these escape mechanisms is of major importance for the prevention, diagnosis and treatment of tuberculosis.

Keywords: Mycobacterium tuberculosis; apoptosis; immune escape; immunology; macrophages.

Figure 1

MTB evasion by inhibiting fusion of lysosomes with phagosomes. While the secretion of PknG by phagocytic MTB directly inhibits the fusion of phagosomes with lysosomes, the suppression of NF-κB also decreases this fusion. As an important component on the phagosome surface, lower biosynthesis and higher hydrolysis of PI3P also suppresses the fusion, providing an escape channel for MTB.

Figure 2

Active (ATBI), latent TB infection (LTBI) or infection granulomas that provide a shelter for bacteria.

Figure 3

Relationship between MHC class II and M. tuberculosis evasion. As non-professional antigen-presenting cells, fibroblasts also present antigen derived from the processing of heat-killed MTB in addition to presenting peptides and isolated proteins. But MTB-infected fibroblasts are unable to present antigen from the bacteria. Peptide-loaded MHC class II molecules activate T cells to generate an immune response against MTB and this action occurs in the plasma membrane. However, PE_PGRS47 expressed by MTB can inhibit the presentation of MHC class II antigen.