Fig. 3

Schematic presentation of aptamer function against different microbial toxins. A) After binding and oligomerization, in the way to create a pore, toxin heptamer inserts into the target cell and leading to cell lysis. In the presence of aptamer, after binding and oligomerization, pore formation does not occur, which inhibit cell lysis. B) *APC: Antigen presenting cell and **SE: Staphylococcal Enterotoxins. SE bound to MHC class II and TCR is expressed on CD⁴⁺ T cells. MHC class II, SEs and TCR interactions may result in hyper activation of the T cells, leading to the excessive proliferation of T cells and the uncontrolled burst of numerous pro inflammatory cytokines and chemokines. Aptamer inhibits T-cell activation, Therefore, the production of cytokines does not occur. C) PA (protective antigen) binds to the Anthrax Toxin Receptor that then interacts with LF to form the lethal toxin. Translocation of LF through the PA heptamer channel into the host cell cytosol results in cell death. Aptamers block the active site of LF and lead to cell survival. D) BONT (botulinum) is internalized into endosomes. In cytosol, proteolysis by the light chain cleavages SNARE proteins (synaptobrevin, SNAP25 and syntaxin) in the neurons and prevents release of the acetylcholine. Aptamers were bounded to light chain of toxin and caused a strong inhibition of endopeptidase activity