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Nano-liposome-based target toxicity machine: an alternative/complementary approach in atopic diseases

, , , , &
Pages 1292-1297 | Received 16 Aug 2016, Accepted 13 Nov 2016, Published online: 29 Nov 2016

Figures & data

Figure 1. An illustrative structure of proposed T-nano-liposome. Liposomes can be surface functionalized to endow stealth through PEGylation and to promote receptor-mediated endocytosis by using targeting ligands such as pollen antigens, SCFV, aptamer, and MIP. PEGylation extends liposomal circulation half-life in vivo by reducing clearance, immune recognition, and the non-specific absorption of serum proteins. Polyethylene glycol (PEG) density determines its structure at the liposome surface.

Figure 1. An illustrative structure of proposed T-nano-liposome. Liposomes can be surface functionalized to endow stealth through PEGylation and to promote receptor-mediated endocytosis by using targeting ligands such as pollen antigens, SCFV, aptamer, and MIP. PEGylation extends liposomal circulation half-life in vivo by reducing clearance, immune recognition, and the non-specific absorption of serum proteins. Polyethylene glycol (PEG) density determines its structure at the liposome surface.

Figure 2. Schematic representation of the steps involved in the nano-liposomes-based target toxicity machine.

Figure 2. Schematic representation of the steps involved in the nano-liposomes-based target toxicity machine.

Figure 3. Scheme of molecular imprinting against CXCl 13. CXCL13 receptors are chosen as a target and an imprint molecule for this hypothesis. The first step is to consider the CXCL13 monomers and template (template is a constant, short peptide sequence illustrative of an available fragment of a larger protein, holes on the template is representative of the active sites in the CXCL13 template). Afterward, all elements of the MIPs are combined and allowed to be self-assembled to form the cross-linked polymer with the template (pre-polymerization). After polymerization, monomers, and the surrounding matrix are cleaved from the template molecules. The resulting targeted MIPs will be able selectively to bind to CXCL13.

Figure 3. Scheme of molecular imprinting against CXCl 13. CXCL13 receptors are chosen as a target and an imprint molecule for this hypothesis. The first step is to consider the CXCL13 monomers and template (template is a constant, short peptide sequence illustrative of an available fragment of a larger protein, holes on the template is representative of the active sites in the CXCL13 template). Afterward, all elements of the MIPs are combined and allowed to be self-assembled to form the cross-linked polymer with the template (pre-polymerization). After polymerization, monomers, and the surrounding matrix are cleaved from the template molecules. The resulting targeted MIPs will be able selectively to bind to CXCL13.

Figure 4. Schematic diagram of B cell activation by allergens and proposed “NBTTM” to eliminate of IgE + B cell from the patients’ body treated with T-nano-liposome.

Figure 4. Schematic diagram of B cell activation by allergens and proposed “NBTTM” to eliminate of IgE + B cell from the patients’ body treated with T-nano-liposome.

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