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. 2019 Aug 12;7(8):255. doi: 10.3390/microorganisms7080255

Figure 1.

Figure 1

Proposed mechanism of action of adjuvants used in subunit tuberculosis vaccine candidate formulations. Many compounds exploit structural features to achieve adjuvanticity (A–C). Liposomal formulations, particularly cationic liposomes (A), protect and retain anionic vaccine antigens whilst creating a depot effect that potentiates slow antigen release. Adjuvant components such as QS21, found in AS01, interact with and disrupt the liposomal membranes (B), enhancing cross presentation to CD8+ T cells and inflammatory cytokine production via the Syk tyrosine kinase pathway. The novel polysaccharide adjuvant, Advax™, (C) potentiates phagocytosis and recruits immune cells to the site of vaccination, despite minimal inflammatory effects. Other adjuvants rely on distinct molecular pathways known to induce inflammation, such as the activation of pattern recognition receptors, both intracellular (Poly:IC (toll-like receptor (TLR)3, TLR7/8, or CpG oligonucleotides (TLR9)) or extracellular (TLR2, 3-O-desacyl-4′-monophosphoryl lipid A (MPLA; TLR4), and Mincle). Chitosan and cyclic dinucleotides (CDNs) activate the cytoplasmic DNA sensor STING.